One of the most promising breakthroughs in the past decade has been immune checkpoint therapy, or simply “immunotherapy.” Immune T-cells continually patrol our body, looking for rogue cells to identify and kill before they can multiply into a tumor. If it weren’t for T-cells, we’d all develop cancer in our twenties. But rogue cancer cells evolve ways to fool cancer-detecting T-cells so they can go on happily multiplying. The latest and most effective immunotherapies bind to proteins on the cancer cells’ surface. It is the equivalent of taking the invisible cloak off cancer cells so T-cells can recognize and kill them. Although fewer than 10 percent of all cancer patients currently benefit from immunotherapy, that number should increase thanks to the hundreds of trials currently in progress.

These theories fit with observations and are generally accepted. Individuals don’t live forever because natural selection doesn’t select for immortality in a world where an existing body plan works perfectly well to pass along a body’s selfish genes. And because all species are resource limited, they have evolved to allocate the available energy either to reproduction or to longevity, but not to both. That was as true for M. superstes as it was and still is for all species that have ever lived on this planet. All, that is, except one: Homo sapiens.

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.

Today, analog information is more commonly referred to as the epigenome, meaning traits that are heritable that aren’t transmitted by genetic means.

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 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.

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.

sirtuins are enzymes that remove acetyl tags from histones and other proteins and, by doing so, change the packaging of the DNA, turning genes off and on when needed. These critical epigenetic regulators sit at the very top of cellular control systems, controlling our reproduction and our DNA repair. After a few billion years of advancement since the days of yeast, they have evolved to control our health, our fitness, and our very survival. 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.

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.

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.

Steve’s name stuck, and today he’s the namesake of the Horvath Clock—an accurate way of estimating someone’s biological age by measuring thousands of epigenetic marks on the DNA, called methylation. We tend to think of aging as something that begins happening to us at midlife, because that’s when we start to see significant changes to our bodies. But Horvath’s clock begins ticking the moment we are born. Mice have an epigenetic clock, too. Were the ICE mice older than their siblings? Yes, they were—about 50 percent older. We’d found life’s master clock winder.

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 often.

Not malnutrition. Not starvation. These are not pathways to more years, let alone better years. 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.

In the meantime, however, almost any periodic fasting diet that does not result in malnutrition is likely to put your longevity genes to work in ways that will result in a longer, healthier life.

You’ll recall that when the enzyme known as mTOR is inhibited, it forces cells to spend less energy dividing and more energy in the process of autophagy, which recycles damaged and misfolded proteins. That act of hunkering down ends up being good for prolonged vitality in every organism we’ve studied. 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.

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. And according to one study funded by the Centers for Disease Control and Prevention and published in 2017, 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.

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.33 That’s a massive effect.

To engage our longevity genes fully, intensity does matter. 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.

as it turns out, exposing your body to less-than-comfortable temperatures is another very effective way to turn on your longevity genes.

Sirtuins are switched on by cold, which in turn activates protective brown fat in our back and shoulders.

Also known as “brown fat,” this mitochondria-rich substance was, until recently, thought to exist only in infants. Now we know that it is found in adults, too, although the amount of it decreases as we age.

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.

Another thing you can try is activating the mitochondria in your brown fat by being a bit cold. The best way to do this might be the simplest—a brisk walk in a T-shirt on a winter day in a city such as Boston will do the trick. Exercising in the cold, in particular, appears to turbocharge the creation of brown adipose tissue.52 Leaving a window open overnight or not using a heavy blanket while you sleep could help, too.

A more convincing study followed a group of more than 2,300 middle-aged men from eastern Finland for more than twenty years.55 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.

None of the sauna studies dug deep enough to tell us why temporary heat exposure may be so good for us. If yeast is any guide, NAMPT, the gene in our bodies that recycles NAD, may be in on the act. NAMPT is turned on by a variety of adversity triggers, including fasting and exercise, which makes more NAD so the sirtuins can work hard at making us healthier.56 We have never tested if NAMPT is turned on by heat, but that would be something to do. Either way, one thing is clear: it does us little good to spend our entire lives in the thermoneutral zone. Our genes didn’t evolve for a life of pampered comfort. A little stress to induce hormesis once in a while likely goes a long way.

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.

Enzymes make life possible by taking advantage of fortuitous molecular movements. Every second you are alive, thousands of glucose molecules are captured within each of your trillions of cells by an enzyme called glucokinase, which fuses glucose molecules to phosphorus atoms, tagging them for energy production. Most of the energy created is used by a multicomponent RNA and protein complex called a ribosome, whose primary job is to capture amino acids and fuse them with other amino acids to make fresh proteins.

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.

Barzilai is leading the charge to make metformin the first drug to be approved to delay the most common age-related diseases by addressing their root cause: aging itself. If Barzilai and his colleagues can show metformin has measurable benefits in the ongoing Targeting Aging with Metformin (TAME) study, the US Food and Drug Administration has agreed to consider aging as a treatable condition. That would be a game changer, the beginning of the end for a world in which aging is “just the way it goes.”

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.

Howitz and I were fascinated by the fact that resveratrol is produced in greater quantities by grapes and other plants experiencing stress. 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. Plants have survival circuits, too, and we think we might have evolved to sense the chemicals they produce in times of stress as an early-warning system, of sorts, to alert our bodies to hunker down as well.

By studying resveratrol, we also learned that it is possible to activate sirtuins with a chemical. This prompted a flood of research into other sirtuin-activating compounds, called STACs, that are many times more potent than resveratrol at stimulating the survival circuit and extending healthy lifespans in animals. They go by names such as SRT1720 and SRT2104, both of which extend the healthy lifespan of mice when given to them late in life.37 There are, today, hundreds of chemicals that have been demonstrated to have an effect on sirtuins that are even more effective than resveratrol’s and some that have already been demonstrated in clinical trials to lower fatty acid and cholesterol levels, and to treat psoriasis in humans.

Another STAC is NAD, sometimes written as NAD+.39 NAD has an advantage over other STACs because it boosts the activity of all seven sirtuins.

Charles Brenner, who is now the head of biochemistry at the University of Iowa, discovered in 2004 that a form of vitamin B3 called nicotinamide riboside, or NR, is a vital precursor of NAD. He later found that NR, which is found in trace levels in milk, can extend the lifespan of yeast cells by boosting NAD and increasing the activity of Sir2. Once a rare chemical, NR is now sold by the ton each month as a nutraceutical. Meanwhile, on a parallel path, researchers, including us, were homing in on a chemical called nicotinamide mononucleotide, or NMN, a compound made by our cells and found in foods such as avocado, broccoli, and cabbage. In the body, NR is converted into NMN, which is then converted into NAD. Give an animal a drink with NR or NMN in it,40 and the levels of NAD in its body go up about 25 percent over the next couple of hours, about the same as if it had been fasting or exercising a great deal.

Every day I’m asked by members of the public, “Which is the superior molecule: NR or NMN?” We find NMN to be more stable than NR and see some health benefits in mouse experiments that aren’t seen when NR is used. But it’s NR that has been proven to extend the lifespan of mice. NMN is still being tested. So there’s no definitive answer, at least not yet.

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.

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.

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. Yes, natural selection is callous, but it works.

That’s what the Mayo Clinic’s James Kirkland has done. 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.4 The implications of this work cannot be overstated. If senolytics work, you could take a course of a medicine for a week, be rejuvenated, and come back ten years later for another course. Meanwhile, the same medicines could be injected into an osteoarthritic joint or an eye going blind, or inhaled into lungs made fibrotic and inflexible by chemotherapy, to give them an age-reversal boost, too. (Rapamycin, the Easter Island longevity molecule, is what’s known as a “senomorphic” molecule, in that it doesn’t kill senescent cells but does prevent them from releasing inflammatory molecules, which may be almost as good.5)

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.

In 2006, the Japanese stem cell researcher Shinya Yamanaka announced to the world that after testing dozens of combinations of genes, he had discovered that a set of four—Oct4, Klf4, Sox2, and c-Myc—could induce adult cells to become pluripotent stem cells, or iPSCs, which are immature cells that can be coaxed into becoming any other cell type. These four genes code for powerful transcription factors that each controls entire sets of other genes that move cells around on the Waddington landscape during embryonic development. These genes are found in most multicellular species, including chimpanzees, monkeys, dogs, cows, mice, rats, chickens, fish, and frogs. For his discovery, essentially showing that complete cellular age reversal was possible in a petri dish, Yamanaka won the Nobel Prize in Physiology or Medicine along with John Gurdon in 2012. We now call these four genes Yamanaka factors.

I predict that cellular reprogramming in the body will first be used to treat age-related diseases in the eye, such as glaucoma and macular degeneration (the eye is the organ of choice to trial gene therapies because it is immunologically isolated).

If adult cells in the body, even old nerves, can be reprogrammed to regain a youthful epigenome, the information to be young cannot all be lost. There must be a repository of correction data, a backup set of data or molecular beacons, that is retained through adulthood and can be accessed by the Yamanaka factors to reset the epigenome using the cellular equivalent of TCP/IP. What those youth markers are, we’re still not sure. They are likely to involve methyl tags on DNA, which are used to estimate an organism’s age, the so-called Horvath clock. They likely also involve something else: a protein, an RNA, or even a novel chemical attached to DNA that we haven’t yet discovered. But whatever they are made of, they are important, for they would be the fundamental correcting data that cells retain over a lifetime that somehow direct a reboot.

Through sequencing, we can even see what kinds of bacteria have managed to make their way into a tumor. Bacteria, it turns out, can protect tumors from anticancer drugs. Using genomics, we can identify which bacteria are present and predict which antibiotics will work against those single-celled tumor protectors.

The same is true of medical interventions: our genes can tell us which are better for us and which could do more harm than good. That’s changing the game for many breast cancer patients. Those who score in a certain range on a genetic test called Oncotype DX, it has been discovered, respond every bit as well to hormone treatments as they do to chemotherapy, the latter of which has far more side effects.5 The tragedy of this discovery is that it didn’t come until 2015. The Oncotype DX test has been in use since 2004, but it wasn’t until a team of researchers decided to take another look at possible treatment options and outcomes that it became clear that the medical community had been subjecting tens of thousands of women to treatments that were more harmful and no more effective.

We need to be constantly challenging the assumptions upon which medical manuals are based. One of these assumptions is that males and females are essentially the same. We’re all too slowly coming around to the shameful recognition that, for most of medical history, our treatments and therapies have been based on what was best for males,6 thus hindering healthy clinical outcomes for females. Males don’t just differ from females at a few sites in the genome; they have a whole other chromosome.

Eventually, every drug will be included in a huge and ever-expanding database of pharmacogenetic effects. It won’t be long before prescribing a drug without first knowing a patient’s genome will seem medieval.

we are about to enter a world in which our genomes will be sequenced, stored, and already red-lighted for treatments that have been demonstrated to have adverse effects on people with similar gene types and combinations as we have.14 Likewise, we’ll be green-lighted for treatments that are known to work for people with similar genes, even if those treatments don’t work for most other people most of the time.

Long wait times aren’t just in the United States, which has a largely private medical system; Canada’s socialized system has notoriously long wait times, too. The problem isn’t how we pay for care; the problem is that we’ve set up doctors as the only conduits to diagnosis and often, in the case of primary care physicians, as the only people who can refer a patient to a specialist. The backlog could clear soon, thanks to technologies that give doctors the ability to conduct video home visits. Within a decade, using a device the size of a package of gum and possibly even disposable, it will be technically feasible to collect the samples your doctor needs at home, plug the device into your computer, and look together at a readout of your metabolites and your genes.

All of this means we’re on the way to a fundamental shift in the way we search for, diagnose, and treat disease. Our flawed, symptom-first approach to medicine is about to change. We’re going to get ahead of symptoms. Way ahead. We’re even going to get ahead of “feeling bad.” Many diseases, after all, are genetically detectable long before they are symptomatic. In the very near future, proactive personal DNA scanning is going to be as routine as brushing our teeth. Doctors will find themselves saying the words “I just wish we’d caught this earlier” less and less—and eventually not at all.

In 2018, a peer-reviewed study published by the team at InsideTracker and me, showed that biotracking and computer-generated food recommendations reduce blood sugar levels as efficiently as the leading diabetes drug, while optimizing other health biomarkers, too.

TECHNOLOGIES TO EXTEND OUR LIVES. In the near future, families will be monitored by biosensing wearables, small devices at home, and implants that will optimize our health and save lives by suggesting meals and detecting falls, infections, and diseases. When an anomaly is found, an AI-assisted, videoconferenced doctor will send an ambulance, a nurse, or medicines to your door.

But by the latter part of the century, the business model that long sustained vaccine research and development was badly broken. The cost of testing new vaccines had risen exponentially, thanks in large part to increasing public concerns about safety and risk-averse regulatory bodies. The “low-hanging fruit” of the inoculation world had already been picked. Now a simple vaccine can take more than a decade to produce and cost more than half a billion dollars, and there is still the chance it won’t be approved for sale. Even some vaccines that have worked well and been critical for the prevention of epidemics, such as GlaxoSmithKline’s Lyme disease vaccine, have been taken off the market because the unfounded backlash against vaccines made continuation of the product “just not worth it.”

The good news is that we are experiencing a minirenaissance in vaccine research and development, which has tripled between 2005 and 2015, now accounting for about a quarter of all biotechnology products being developed.39 The big one is malaria, infecting 219 million people and claiming 435,000 people in 2017.40 Thanks to Bill and Melinda Gates, GlaxoSmithKline, and Program for Appropriate Technology in Health (PATH), a partially effective vaccine against malaria known as Mosquirix was deployed for the first time in 2017, giving hope that the malaria parasite will one day be pushed to extinction.

Now, as we rapidly approach the era of self-driving cars—a technological and social paradigm shift that almost every expert expects will rapidly reduce car crashes—we need to confront an important question: Where will the organs come from?

Soon it won’t matter if the morbid pipeline for human organ transplantation ends. That pipeline never met the demand anyway. In the future, when we need body parts, we might very well print them, perhaps by using our own stem cells, which will be harvested and stored for just such an occasion, or even using reprogrammed cells taken from blood or a mouth swab. And because there won’t be competition for these organs, we won’t have to wait for things to go catastrophically wrong for someone else to get one—we’ll only have to wait for the printer to do its job.

Once people begin to accept that aging is not an inevitable part of life, will they take better care of themselves? I certainly have. So, too, it seems, have most of my friends and family members. Even as we have all stepped forward to be early adopters of biomedical and technological interventions that reduce the noise in our epigenomes and keep watch over the biochemical systems that keep us alive and healthy, I’ve noticed a definite tendency to eat fewer calories, reduce animal-based aminos, engage in more exercise, and stoke the development of brown fat by embracing a life outside the thermoneutral zone.

“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

economist Harun Onder is among those who have made a demographic observation: nationalist arguments tend to resonate with older people.27 Therefore, it is likely that the antiglobalist wave will be with us for some time to come. “Virtually every country in the world,” the United Nations reported in 2015, “is experiencing growth in the number and proportion of older persons in their population.” Europe and North America already have the largest per capita share of older persons; by 2030, according to the report, those over the age of 60 will account for more than a quarter of the population on both of these continents, and that proportion will continue to grow for decades to come. Once again, these are estimates based on ridiculously low projections for lengthened lifespans.28

On a plane from Boston to Tokyo recently, I introduced myself to a man sitting next to me and we chatted about our work. When I told him that I was endeavoring to extend human lives, he curled his upper lip. “I don’t know about that,” he said. “It sounds unnatural.” I gestured for him to look around. “We are in reclinable chairs, flying at six hundred miles an hour seven miles above the North Pole, at night, breathing pressurized air, drinking gin and tonics, texting our partners, and watching on-demand movies,” I said. “What about any of this is natural?”

Humans just happen to be a species that excels at acquiring and passing on learned skills. In the past two hundred years, we have invented and utilized a process called the scientific method, which has accelerated the advancement of learning. In this way of thinking, then, culture and technology are both “natural.” Innovations that permit us to feed more people, to reduce disease, and, yes, to extend our healthy lives are natural.

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.

Pessimism, it turns out, is often indicative of exceptional privilege. When viewed globally, however, it gets a lot harder to make the case that the world is an increasingly miserable place. It’s simply not.

There are several ways to speed innovation to find and develop medicines and technologies that prolong healthy lifespan, but the easiest is also the simplest: define aging as a disease. Nothing else needs to change. Researchers working on aging will compete on equal footing with researchers working to cure every other disease in the world. The science-based merits of grant proposals will dictate which research efforts are funded. And private investment will continue, as it should, to drive innovation and competition.

Having seen what works, other, mostly European countries have adopted similar health care systems. Australia now has reciprocal agreements with the United Kingdom, Sweden, the Netherlands, Belgium, Finland, Italy, Ireland, New Zealand, Malta, Norway, and Slovenia, which means that citizens from those countries can receive the same medical care in Australia as they can at home, and vice versa. Imagine an entire world like that.

At least in one regard—the “stuff factor,” so to speak—technology is already driving a tremendous and positive change, a global process of “dematerialization” that has replaced billions of tons of goods with digital products and human services. Thus it is that wall-to-wall shelves dedicated to records and compact discs have been replaced by streaming music services; people who once needed vehicles for once-in-a-while travel now open an app on their phones to request a ride share; and entire wings of hospitals once used for storing patients’ records have been supplanted by handheld cloud-connected tablet computers.

Labor leaders, meanwhile, are locked in an understandable but ultimately futile fight for retirement and benefits for workers who in the past would have labored for forty or fifty years, retired for a short spell, and then rather promptly died. Almost no one is fighting over what the world of work will look like when age is truly nothing more than a number.

what do I do? • 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. • 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.