CONCLUSION
LET ME TAKE YOU ON a tour of my lab at Harvard Medical School in Boston, Massachusetts.
You’ll find us in the Genetics Department in the New Research Building, arguably the best group of biologists in the world. That’s the same place where Connie Cepko is working to grow mammalian eyes in a dish and studying the potential for gene therapy to restore lost vision. Down the hall in his clean room, David Reich, the author and scientist, is sequencing DNA from 20,000-year-old teeth and discovering that our ancestors liked to breed with other human subspecies. And a floor down, George Church is working on, among other wizardries, printing an entire human genome and reviving the woolly mammoth. Across the street, Jack Szostak has moved on from his Nobel Prize–winning work to uncover secrets about how life began four billion years ago; he comes by sometimes to visit.
Yeah, the elevator conversations are awesome.
My lab is on the ninth floor. The first person you’ll see when you walk in the office is Susan DeStefano, who basically has kept our lab and my life under control for the past fourteen years. Susan is a devout Christian who believes in the literal version of Genesis. She figures that we are doing God’s bidding by helping the sick and the needy; there’s no reason why our views on God and science can’t coincide. We both want to make the world a better place.
To the left of Susan’s doorway you’ll find lab manager Luis Rajman’s office. Luis, who has a PhD in cellular and molecular biology, ran the transgenic mouse facility at the giant biotech company Biogen Idec, but when we first met he was managing a high-end framing company. He’s worked on paintings worth more than my house—and probably more than all my neighbors’ houses together, too—so he’s the right sort of guy for a job that requires exceptional meticulousness. Sitting with her back to Luis is Karolina Chwalek, who has a PhD in regenerative medicine and is our chief of staff, a strict but fair manager who makes sure our team of thirty to forty scientists is funded and remains very much worth funding.
Daniel Vera sits next to Luis and is usually staring at at least one and often several screens. He’s the lab’s data guru, having established Florida State University’s Center for Genomics. I’ll never forget the day he showed me the whole-genome analysis of the epigenetic changes in the ICE mice that helped reinforce the Information Theory of Aging.
Down the hall, past framed copies of research papers we’ve published, there’s a sign above a door that says “Operations Room,” as a nod to Winston Churchill’s central command. Inside you’ll find the lab and an ever-rotating group of some of the best minds in the world. When I took a walk through the lab on one recent day, one of my favorite things to do, these were some of the characters who were there.
On my left were Israel Pichardo-Casas, a Mexican cell biologist, and Bogdan Budnik, a Ukrainian physicist, who have found more than five thousand new human genes within noncoding “junk DNA.” These small genes make small proteins that course through our bloodstreams, any one of which could be a treatment to cure cancer, treat diabetes, or be the factor that allows young mice to rejuvenate the old. Then there were the Michaels: Bonkowski, Schultz, and Cooney. Bonkowski played a key role in our study on reversing vascular aging, making old mice run twice as far.1 He holds the record for the creation of the longest-lived mouse in scientific history, at five years.
Schultz, his mentee, is studying the molecular events that cause age-related inflammation, looking for ways to suppress that reaction and thus remove a key driver of age-aggravated diseases. He and Bonkowski are using gene therapy to “infect” old mice with longevity genes, aiming to break their own mouse longevity record.
Cooney is working with NASA to introduce DNA repair genes—from the supertough, eight-legged micro creatures known as tardigrades—into human cells in an effort to provide astronauts with protection from cosmic radiation and, of course, to slow aging.
There was João Amorim from Portugal; he’s studying resveratrol and a bunch of STACs in an effort to understand how they activate SIRT1 in the body. He’s changed just one base pair in the mouse SIRT1 gene that makes the enzyme resistant to resveratrol and other STACs. He’s testing if that mutant mouse still receives the health and lifespan benefits of resveratrol. If resveratrol no longer works on the mutant, then it should resolve the debate about whether resveratrol is working by directly activating the SIRT1 enzyme, or via some other mechanism, like activating AMPK. So far, the results look promising for the SIRT1-activation hypothesis.
There was Jae-Hyun Yang from South Korea; he has spent the past six years tickling the chromosomes of cells and animals to understand how and why the ICE mice age prematurely. It was he and João who first showed that the epigenetic clock in the ICE mice ticks faster. Next to him was Yuancheng Lu, one of China’s top students, who discovered the powerful epigenetic reprogramming system that can be delivered into aged animals via a modified virus.
Xiao Tian had just used that virus to protect human nerve cells from chemotherapy. The normal nerves had either died or shrunk into a ball. But the reprogrammed ones were completely healthy, with long, beautiful cellular projections extending out across the floor of the petri dish. Some experiments aren’t very conclusive; this was night and day. We plan to test our virus in patients with eye disorders within a couple of years.
Patrick Griffin, my most recent graduate student, wants to know if stimulating a response to DNA damage, without creating actual DNA damage, is sufficient to cause aging in mammals. To test this, he has designed a way to tether DNA damage signaling proteins to the genome using a non-cutting version of Cas9/CRISPR. If our theory is correct, he should still cause aging. Jaime Ross has engineered “NICE mice” to experience accelerated epigenomic noise just in neurons. She wants to know if the brain controls aging in the rest of the body, and if these mice operate more like eighty-year-old humans. If so, they could be used as better models for human brain aging and possibly Alzheimer’s disease.
Joel Sohn has worked with some of the greatest biologists of the twentieth century, then spent thirty years as a fisherman catching and exporting marine life, and is now searching the seas for secrets of immortality. He’s studying cnidarians, transparent ocean animals that can do amazing tricks with their bodies, such as regrow a new body part or spawn a baby from their feet. That day was a good day for Joel: his decapitated sea anemone was regrowing a head, and his immortal jellyfish were budding off baby clones. Perhaps these regenerative processes are the same as the ones that allow us to regenerate optic nerves. Perhaps these creatures have access to the biological equivalent of Shannon’s observer, the one who stores youthful epigenetic information.
Abhirup Das, who spearheaded the old mouse marathon project, was studying the impact of precursors such as hydrogen sulfide and NMN on wound healing. Lindsay Wu, who also runs our labs in Sydney, Australia, at the University of New South Wales, was examining molecules that activate an enzyme called G6PD, which has been shown to extend the lifespans of multiple animals and, tragically, is mutated in 300 million people, the most common of all mutations. He has also restored fertility in old female mice by feeding them NMN and protecting their eggs from DNA damage.
There was our resident dental student, Roxanne Bavarian, who is working to identify the role of sirtuins on oral toxicities and cancer. And there was Kaisa Selesniemi, from Finland, who is one of the world’s leading experts on culturing stem cells from ovaries and reversing female infertility.
Parvez Mohammed, from India, was creating new chemicals in the fume hood, and Conrad Rinaldi was testing if the latest batch worked to rejuvenate skin cells from aged people. Giuseppe Coppotelli, from Italy, was examining new human longevity genes we’d discovered, including one called Copine2 that is mutated in Parkinson’s and Alzheimer’s disease patients.
Alice Kane, an Australian, was examining some mice to develop a mouse frailty clock to predict how long a mouse will live and is helping all of us see and appreciate sex differences. Jun Li, our lab’s senior biochemist, was investigating why our ability to repair DNA goes down with age and has found that NMN reverses the process.2
And those were just the people who were in the lab on that specific day. There are others—a lot of them—who are doing world-changing work.
These people are brilliant. They could be working on answering any question in the universe. But they’ve come to Harvard to work on aging. Some of them are introverts, as scientists often are. A few are cautious, conservative researchers, a trait I’m working to fix. Yet there isn’t a single one who doesn’t believe that prolonged human vitality is on its way.
And this is just one lab. There are three more labs in the Paul F. Glenn Center for the Biology of Aging at Harvard that are focused on helping people live longer and healthier lives. At Bruce Yankner’s lab, they’re exploring the impact of aging specifically on the human brain. Marcia Haigis’s lab is investigating the role that mitochondria play in aging and disease and has uncovered the role of sirtuin mutations in cancer. Amy Wagers’s lab was one of the first to show the blood of young mice rejuvenates the old, and vice versa, prompting people to infuse themselves with serum from young donors. Amy and I are collaborating to find the factors in the blood and develop new, advanced pharmaceuticals to treat age-related diseases without the creepiness.
At another Glenn Center, just across the river at MIT, Lenny Guarente, Angelika Amon, and Li-Huei Tsai are all working on fundamental questions related to slowing, stopping, and reversing aging. In other cities in the United States, Thomas Rando, Anne Brunet, Tony Wyss-Coray, Elizabeth Blackburn, Nir Barzilai, Rich Miller, and others are all running large labs or centers aimed at changing the way we think about aging. North of San Francisco there is an entire building, called the Buck Institute for Research on Aging, completely devoted to understanding and combating aging. The list goes on and on.
Those are just a few of the labs. Around the world, more than a dozen independent research centers are working hard on these same questions, and there is now at least one scientist in every major university in the world who is working on aging. Most of these labs obtain their research grants for other diseases but increasingly are turning their attention toward understanding aging, reasoning that fixing that problem will fix whatever disease they’re funded to fight. This is, after all, an environment in which a huge source of research funding is off limits for those who are fighting something that most people believe is inevitable and few people recognize is a disease.
Meanwhile, private enterprise is leading the way in the development of neural net-based initiatives for drug discovery and development, gene analysis, biotracking, and disease detection to dramatically extend our lives. And every day research into the simple things anyone can do to prolong their lifespans and healthspans is mounting, too—offering better and better maps to good health and long lives.
A decade or two ago, when even the most optimistic scientists were only just beginning to envision a world in which aging wasn’t inevitable, and when there were only a handful of researchers in the world specifically working to slow, stop, or reverse aging, I certainly could understand when people listened politely about my work and then gave me a look as though I were crazy. Today I have a hard time understanding how anyone could look at this vast and brilliant army of researchers and not believe that a tremendous change in human aging is coming—and soon.
I have some compassion for those who say “It can’t be done.” They are, in my view, the same kind of people who said vaccines couldn’t work and humans couldn’t fly. But given the benefits that longevity research can bring to the world, I have far less patience—indeed, really none at all—for those who say “It shouldn’t be done.”
BEYOND BELIEF
There are those who would have you believe that the people in my lab—and those like them in labs around the world—are engaged in an unnatural and even immoral campaign to change what it means to be human. That view is rooted in ideas about human nature that might charitably be described as subjective but that are probably more accurately called zealotry.
That, it seems to me, was the guiding force behind a 2003 report submitted to the White House by the President’s Council on Bioethics entitled Beyond Therapy: Biotechnology and the Pursuit of Happiness, which ominously warned against aging research because it goes against “the human grain” and violates the purportedly orderly cycle of birth, marriage, and death.
Would people “be more or less inclined to swear lifelong fidelity ‘until death do us part,’ if their life expectancy at the time of marriage were eighty or a hundred more years, rather than, as today, fifty?”3 the council wondered. What kind of unhappy marriages, I wondered in return, would drive people to even ask such a question? I would love to have an extra fifty years with my wife, Sandra.
Aging, the council proffered, “is a process that mediates our passage through life, and that gives shape to our sense of the passage of time”; without it, the council’s members cautioned, we could become “unhinged from the life cycle.”4
Our so-called natural life cycle, of course, is one in which the vast majority of our ancestors never got old enough to get gray hair or wrinkles and in which consumption by carnivore was a perfectly ordinary way to go. If you’d like to be hinged to that, be my guest.
“Might we be cheating ourselves,” the council asked, “by departing from the contour and constraint of natural life (our frailty and finitude), which serve as a lens for a larger vision that might give all of life coherence and sustaining significance?”5
Oh, for goodness’ sake, if we truly believed that frailty was a requisite for meaningful life, we’d never mend a broken bone, vaccinate against polio, or encourage women to stave off osteoporosis by maintaining adequate calcium levels and exercising.
I know I shouldn’t get worked up about these sorts of things. It’s a tale as old as science, after all—just ask Galileo what happens when you “disrupt the natural order of things.”
But this was more than a trifling report from moralizing bureaucrats. The chair of the committee that wrote it, Leon Kass, is one of the most influential bioethicists of our time and came to be known, during the tenure of George W. Bush, as “the President’s Philosopher.” For years after the report was issued, aging research was framed not as a fight against a disease but as a fight against our humanity. That’s hogwash, and, in my mind, it’s rather deadly hogwash.
Yet once the framing has been set, the effort to shift ideas, understandings, and biases becomes a herculean one. The fight to help people see aging for what it is, rather than “just the way it goes,” will be a long one.
More funding for the kind of research happening in my lab and others like it could bring about these advancements even sooner. But because of a lack of funding, people over sixty today may not live long enough to be helped. If you and your family members end up the last of humanity to live a life that ends all too early with decay and decrepitude, or our children never see the benefits of this research, you can thank those bioethicists.
After all of these arguments, if you still think that extending the healthy part of your life would not be for you—perhaps it would reduce your life’s urgency or be against the natural course of things—consider your friends and family. Would you subject your loved ones to a decade or two of unnecessary hardship having to look after you physically, emotionally, and financially in your final years if you didn’t have to?
Spend a day in a nursing home like my wife does every few days. Go feed people who can’t chew. Wipe their bottoms. Bathe them with a sponge. Watch as they struggle to remember where they are and who they are. When you are done, I think you will agree that it would be negligent and cruel for you not to do what you can to combat your own age-related deterioration.
There are still a lot of people like Kass out there. But if they live long enough, they will also have to come to terms with reality. The momentum makes the future I have described, or one close to it, unstoppable. Prolonged healthspans are inevitable.
More and more people recognize this every day, and they want in.
Because no matter what people say or believe, whether they are optimists or scaremongers, scientists or bioethicists, there is change in the air.
On June 18, 2018, WHO released the eleventh edition of the International Classification of Diseases, known as ICD-11. It is a fairly unremarkable document, except that someone slipped in a new disease code. At first no one saw it. Here is the line, which you can find on the WHO website6 if you type in code MG2A. It reads:
MG2A Old age
• old age without mention of psychosis
• senescence without mention of psychosis
• senile debility
Every country in the entire world is encouraged to start reporting using ICD-11 on January 1, 2022. What this means is that it is now possible to be diagnosed with a condition called “old age.” Countries will have to report back to the WHO with their statistics on who dies from aging as a condition.
Will this lead to changes at the regulatory level, directing billions of dollars in investment to develop the medicines we deserve? Will federal regulators and doctors finally accept that it is ethically okay to prescribe medicines to slow aging and all the diseases that aging causes? Will they recognize it is indeed within a patient’s rights to receive them? Will insurance companies reimburse patients for the cost of antiaging treatments that will save money down the line?
We will see. I certainly hope the winds build. Until that time comes, though, there is plenty we can do.
WHAT I DO
Save for “Eat fewer calories,” “Don’t sweat the small stuff,” and “Exercise,” I don’t give medical advice. I’m a researcher, not a medical doctor; it’s not my place to tell anyone what to do, and I don’t endorse supplements or other products.
I don’t mind sharing what I do, though, albeit with some caveats:
• This isn’t necessarily, or even likely, what you should do.
• I have no idea if this is even the right thing for me to be doing.
• While human trials are under way, there are no treatments or therapies for aging that have been through the sort of rigorous long-term clinical testing that would be needed to have a more complete understanding of the wide range of potential outcomes.
People often wonder, when I tell them things like this, why on earth I would subject myself to the potential for unexpected and adverse side effects or even the possibility—low though it seems to be—that I could expedite my own demise.
The answer is simple: I know exactly what is going to happen to me if I don’t do anything at all—and it’s not pretty. So what do I have to lose?
And so, with all that on the table, 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.
About fifty times a day I’m asked about supplements. Before I answer, let me say that I never recommend supplements, I don’t test or study products, nor do I endorse them; if you see a product implying that I do, it’s certainly a scam. Supplements are far, far less regulated than medicines, so if I do take a supplement, I look for a large manufacturer with a good reputation, seek highly pure molecules (more than 98 percent is a good guide), and look for “GMP” on the label, which means the product was made under “good manufacturing practices.” Nicotinamide riboside, or NR, is converted to NMN, so some people take NR instead of NMN because it is cheaper. Cheaper still are niacin and nicotinamide, but they don’t seem to raise NAD levels as NMN and NR do.
Some people have suggested NAD boosters could be taken with a compound that provides cells with methyl groups, such as trimethylglycine, also known as betaine or methylfolate. Conceptually, this makes sense—the “N” in NR and NMN stands for nicotinamide, a version of vitamin B3 that the body methylates and excretes in urine when it is in excess, potentially depleting cells of methyls—but this remains a theory.
My father follows almost the same regimen as I do, and I can’t remember the last time he was sick. He claims he’s speeding up. This summer, he left his busy social calendar behind in Australia, and, having helped us with home repairs in Boston for six weeks while working remotely in his second career at the University of Sydney, he then drove around the US East Coast for a few weeks with his lifelong friend on their annual pilgrimage to the Summer Theater Festival in Wooster, Ohio.
Dad flew home at the end of summer, only to come back a few weeks later to see me get “knighted,” as he called it, in Washington, DC. Now that he’s home in Sydney again, he’s planning on driving six hundred miles north for a few days to “see a couple of friends.” He is loving life, seemingly more than he ever has.
As I get older, I spend more and more time thinking how lucky I’ve been in life. As an Aussie, I was taught that “big boys don’t cry.” But, nowadays, when I have the time and the sense to pause for a few moments to ponder my life, it’s easy to get a little teary.
I grew up in a free country, then moved to an even freer one. I have three amazing children and friends who treat my family like their own. I am very proud of Sandra, my wife, who was one of the top students in Germany. She aced her botany degree, then came to Boston to be with me, got into the PhD program at MIT, and worked in a lab that was cloning mice for the first time. To earn her PhD, she figured out how to cure mice of a lethal genetic disease called Rett syndrome that disrupts the epigenome and prevents brain development in infant girls. By strange coincidence, the gene she worked on, MECP2, binds to methylated DNA and might be a cellular observer that stores youthful age correction data.
Sandra has been teaching me a lot these past twenty-five years about how to be a better husband and parent, not to mention the names of all the plants, insects, and animals we see on our walks. When we were first married, we argued a lot. She had “ethical issues” with my research, which pained me. Now, having examined and discussed the wealth of biological and economic data over the years, we no longer argue as much, and in fact she’s started taking NMN.
It’s impossible to say if my regimen is working for us, but it doesn’t seem to be hurting. I am now 50, and I feel the same as I did when I was 30. My heart looks 30, too, according to a video of my heart in 3D that one of my colleagues kindly made by inserting me into an experimental magnetic resonance imager. I don’t have a gray hair, and I’m not superwrinkly—well, at least not yet.
A year ago, my younger brother, Nick, was going gray and losing his hair when he demanded to be put on the same regimen after accusing me, only half jokingly, of using him as a negative control. I insisted that I would never do that to my own brother, but I can’t say the thought hadn’t crossed my mind. He’s now on my dad’s regimen, too.
Living longer makes no sense if you don’t have your friends and family around you. Even our three dogs—a small 10-year-old poodle cross named Charlie and two 3-year-old black Labradors, Caity and Melaleuca—have been on NMN for a couple of years. Charlie is a therapy dog whose job it is to calm people, but he becomes too hyperactive if Sandra gives him NMN the day he heads to work, so on those days he’s off it. Caity suffers from a congenital kidney defect, and we hope NMN will allow her to make it past her predicted five-year expiry date. The results of tests in mice with kidney damage say it’s possible.8
A lot of people think a regimen intended to promote prolonged vitality must be hard to stick to, but if it were, my family couldn’t do it. We are just an average bunch trying to get through the day. I do live life as mindfully as possible, focus on feeling good, and check my blood markers occasionally. Over time, I’ve identified the diet, exercise, and supplement routines that work best for me. And I’m confident that my family and I will continue to fine-tune these practices in response to the evolving research as our lives go on.
And on.
And on.
Because, yes, I do hope to be here for a long time to come. There are plenty of X factors that could interfere with that goal. I could get hit by a bus tomorrow, after all. But it’s getting easier and easier to imagine being around—happy, healthy, and connected to friends, family members, and colleagues—past my 100th year.
How long past my 100th year?
Well, I think it would be nice to see the twenty-second century. That would mean making it to my 132nd year. To me, that is a remote chance but not beyond the laws of biology or way off our current trajectory. And if I do make it that far, perhaps I’ll want to stick around even longer.
There’s so much I want to do—and so many people I’d like to help. I’d love to keep nudging humanity down what I believe is a path to greater health, happiness, and prosperity, and to live long enough to know what path we take.
BUSHWALKING. If you head north from my childhood home, you’ll move through hundreds of miles of consecutively larger national parks, a seemingly endless undulation of saltwater estuaries and craggy mountain ridges decorated by ancient rock carvings left by the original inhabitants, the Garigal clan. Dad is now 80, the age his mother, Vera, was when she lost the will to live—aging has that effect on people. Instead, my father hikes mountains, travels the world, and has started a new career, representing hope for all of us.
BUSHWALKING
I recently returned to the neighborhood where I grew up, in the northern suburbs of Sydney, on the edge of Garigal National Park. Dad and Sandra were both there, and so was my twelve-year-old son, Benjamin.
We’d come for a hike along the trail, the exact same one my grandmother Vera used to take my brother and me on when we were that age. She’d tell us stories about her difficult childhood, about how lucky we were to have grown up in a free country, and about the wisdom of A. A. Milne:
“What day is it?” asked Pooh.
“It’s today,” squeaked Piglet.
“My favorite day,” said Pooh.
Dad was raring to go. Ben was, too. Tigers, those boys are. But as I stood at the beginning of the trail, on the edge of a high sandstone cliff overlooking a gully filled with ambrosial eucalyptus and with deafening cicadas overhead, I found myself frozen in awe by the way in which the city quickly gave way to the bush, how the present and the deep past came together, and how it felt to be on the edge of something so vast and so beautiful.
If you wind your way south, down the rocky trail leading off Melaleuca Drive, the street I lived on as a boy, you’ll reach Middle Harbor, an estuary lined by a canopy of bloodwoods, angophoras, and scribbly gum trees that ends in Sydney Harbor. If instead you head north, you’ll move through hundreds of miles of consecutively larger national parks: Garigal to Ku-ring-gai to Marramarra, Dharug to Yengo to Wollemi, a seemingly endless undulation of saltwater estuaries and craggy mountain ridges decorated by ancient rock carvings. You could walk for days, even for weeks, and not hear anyone, save for the distant echoes of the original inhabitants of this land.
On that day in Garigal Park we were planning on walking only a few hours, but I’d been looking forward to it for weeks.
There is, at least to me, a subtle but important difference between hiking and bushwalking. When people hike, they are most often looking for exercise, serenity, beauty, or time together with loved ones. When Australians go for a bushwalk, they are seeking all of those things but with the intention of finding wisdom, too.
I’m not sure how long I was standing on the cliff. A minute or two, perhaps. Five or ten, maybe. However long it was, my family didn’t seem to mind. When the spell of nostalgia and wonderment released me, I found them a short way down the trail.
Ben was peeling the paperlike bark off a melaleuca tree, while Dad was trying to explain something to him about the cliffs being made of sand that had been deposited when mammals first appeared. Sandra was examining a banksia—the strange, prickly flower Sir Joseph Banks collected to show the Royal Society—which, she delighted in reminding us, for the umpteenth time, is a member of the Proteacea family.
As I write this, Ben is in seventh grade. He’s a good boy. A smart boy. He wants to work in my lab someday and take over from me to “finish the job.” I tell him he’ll have a lot of competition and won’t get any special treatment from me, and he says, “Well, if that’s true, I can always work for Lenny Guarente.”
Yes, he’s a funny boy, too.
Our two older children are making their own paths: Natalie, I reckon, as a veterinarian; Alex, perhaps, as a diplomat or a politician.
Dad is now 80, the age his mother, Vera, was when the fire in her eyes had completely gone. She had lost the will to live and never ventured outside again. I cannot predict the future, but when I look at the full life Dad leads now, his world travel, his optimism, and the state of his health, I think he’ll be around for a long time to come. I sure hope he will.
Not just because he represents hope for all of us, but because I’d like to come back to this place again and again with Dad and Sandra and all those I love. Searching for serenity. Hearing stories. Finding beauty. Making memories.
Sharing wisdom.
With Ben and Natalie and Alex, yes. But also with their children. And with their children’s children.
Why not? Nothing is inevitable.