Introduction
Summary of the Book Ending Aging by Aubrey de Grey. Before moving forward, let’s take a quick look at the book. Welcome to a world where the very nature of aging is called into question. In these chapters, you’ll explore a remarkable idea: that the steady decline we’ve always accepted as normal might not be inevitable. As you read, imagine unlocking the secrets behind cellular damage, mitochondrial mutation, and the unwanted protein clumps clogging our tissues. Picture a future where diseases long linked to old age are no longer guaranteed, and where careful medical engineering extends human vitality beyond known horizons. You will meet concepts that push the boundaries of science—from gene therapies and stem cell treatments to ingenious strategies for clearing out harmful byproducts inside our bodies. Each step taken in understanding and overcoming aging leads us closer to a world in which staying healthy and youthful may become a genuine choice.
Chapter 1: Challenging the Ancient Belief that Aging is Completely Unavoidable and Destined by Nature.
For countless generations, people have believed that growing older is as inevitable as the sunrise. We watch our grandparents slow down, their hair turning gray, their joints stiffening, and their memories fading. This common experience leads us to assume that aging is a natural and unalterable law of life. But what if this long-held conviction is only part of the story? Some forward-thinking scientists and researchers are daring to suggest that aging might be more like a technical problem that can be solved, rather than an absolute fate we must accept. Instead of treating aging like an unstoppable force of nature, what if we saw it as a collection of challenges inside our bodies—challenges that we can understand, manage, and maybe even reverse? By viewing aging as a puzzle, we might discover surprising possibilities that were once considered pure fantasy.
Imagine opening your eyes to a future where becoming old and frail is no longer a given, but a choice to be delayed or avoided. The traditional view says we must eventually fall apart and perish, but modern thinkers are assembling a toolkit of emerging therapies and medical technologies that challenge this gloomy perspective. For instance, the British biomedical gerontologist Aubrey de Grey proposes that since aging results from various forms of damage building up in our bodies, we could learn to remove or fix that damage. This might sound like science fiction, but it’s rooted in serious biology and engineering principles. From this viewpoint, halting aging is not about breaking nature’s laws; it’s about applying human creativity and reason to maintain our cellular machinery indefinitely.
Historically, we’ve just accepted aging because we haven’t known a better alternative. Our ancestors didn’t understand cells, DNA, or the complex chemistry that keeps our organs functioning. Without the knowledge or tools to slow deterioration, aging seemed like destiny. Now, we live in a time when scientists are diving deep inside our tissues, exploring every tiny structure, and learning how they wear out over time. Many experts now argue that since aging is driven by understandable biological processes—like cells accumulating faults and waste products—we might be able to repair them. With these insights, aging becomes less of a towering mystery and more like a systematic problem, similar to rust in a machine. If we’ve learned to maintain cars and computers, why not the human body, too?
In fact, there already exists a roadmap to tackling the root causes of aging, known as SENS (Strategies for Engineered Negligible Senescence). This approach treats aging as the gradual buildup of damage that can be repaired before it spirals out of control. By approaching aging as a technical challenge, SENS scientists imagine a future where the idea of growing old is not about slipping into weakness and decline, but rather about staying functional and energetic for much longer. Their methods range from fixing cell parts damaged by free radicals to cleaning up harmful protein clumps in our brains, all with one incredible goal: to prevent the steady downward slide we call aging. Step by step, this program aims to transform aging from an unchangeable fate into a manageable condition.
Chapter 2: Moving Beyond Prevention and Cure Toward the Bold Concept of Body-Wide Repair Strategies.
When dealing with an illness, we usually think in terms of prevention or cure. If you want to avoid heart disease, you might exercise and follow a healthy diet (prevention). If you get sick anyway, you take medicines to heal (cure). But when it comes to aging, these old categories don’t fit so neatly. Aging is complicated, caused by countless tiny damages accumulating over time. Trying to prevent every aspect of aging seems impossible—there are too many factors. Attempting to cure aging directly isn’t straightforward either, since aging isn’t one disease but a bundle of ongoing, widespread harm throughout the body. This complexity leaves us seeking a new approach. The innovative idea: focus on repair. Instead of preventing or curing aging all at once, we could fix the damage as it arises.
Think about an old car: over the years, it rusts, parts wear down, fluids leak, and filters clog. You can’t simply prevent all wear and tear by driving carefully. Nor can you cure old car syndrome with a single magic potion. But you can repair the car regularly—replacing brake pads, changing the oil, fixing dents—so it runs as if it were much younger. Aging bodies are like that old car, and a repair strategy aims to find each source of damage and mend it. If we learn to do this systematically, we might halt or even reverse the clock on our physical decline. This is more than wishful thinking; it’s a shift in perspective that could let middle-aged people regain vitality and carry it forward into old age.
Let’s consider a hypothetical 40-year-old person. If we tried prevention, and somehow slowed aging by half, this person, expected to live until about 80, might make it to 120. That’s impressive, but it still only adds extra decades onto the end. On the other hand, if we focus on repair, removing the damage that’s built up so far at 40, and keep doing so regularly, by the time the person reaches what would have been their normal old age at 80, their body might still resemble that of a vibrant 50-year-old. Continued treatments could push this lifespan much further, perhaps far beyond anything we now consider normal. Repairing damage, rather than merely slowing its accumulation, might multiply our healthy years and revolutionize the idea of human longevity.
This daring concept suggests a future where living to 100 or 150 in good health isn’t shocking. It would require a shift from today’s medicine—which often treats diseases after they appear—to a proactive maintenance model that addresses damage before it becomes debilitating. While some may question whether humanity is ready for such changes, the logic is straightforward: by treating aging not as an unstoppable reality, but as a manageable condition, we grant individuals the possibility of more productive years. It’s about breaking free from the resignations of the past and embracing a medical approach that sees aging as something we can tackle head-on. Armed with such an outlook, we stand on the brink of a new era where advanced therapies keep our bodies working smoothly, decade after decade.
Chapter 3: Unraveling the Hidden Enemy Within Our Cells—Mitochondria and Free Radical Damage.
Deep inside each of our cells, tiny power plants called mitochondria generate the energy that keeps us alive. They process nutrients and oxygen to produce the fuel we need to move, think, and grow. But like any power plant, this process creates byproducts. Chief among these troublesome leftovers are free radicals—reactive molecules missing an electron that eagerly snatch electrons from other molecules, causing a ripple of damage. Over time, this chain reaction can harm our cellular structures, including DNA. Damaged mitochondrial DNA can cause errors in how cells run, making them age faster or function poorly. This silent sabotage, happening millions of times within our cells, is a key factor in why our bodies gradually wear down and lose their youthful resilience.
If we think of our cells as bustling cities, mitochondria are like factories producing energy. But their waste—free radicals—act like unstable vandals. Normally, cells try to control these vandals by using antioxidants and repair mechanisms. However, not all free radicals are caught, and over the years, the damage accumulates. This wear and tear on mitochondrial DNA can lead to errors that spread as cells divide, weakening tissues and organs. It’s similar to how a small crack in a house’s foundation can eventually threaten the whole structure. Understanding this process helps us see that aging isn’t random. It’s driven by well-defined chemical reactions that we might learn to manage, and possibly even halt, through clever interventions targeting these cellular troublemakers.
One hopeful solution to mitochondrial damage is called allotopic expression. This is like making a backup copy of your most important files and storing them in a safer place. Normally, mitochondrial DNA sits right next to the free radical source, making it vulnerable. Allotopic expression means placing copies of key mitochondrial genes into the cell’s main nucleus, a better-protected vault. Inside the nucleus, these genes are sheltered from the constant barrage of free radicals. When a cell uses these backup genes to produce essential proteins, it reduces the chance that damaged mitochondrial DNA will cause serious problems. Although this technique is still under development, it represents a clever approach: if we cannot fully stop free radicals, we can at least shield our genetic blueprints from their destructive reach.
This line of research shows us that the monsters lurking in our cells are not invincible. With the right strategies, we can block their harmful actions or outsmart their attempts at causing damage. Mitochondrial repair strategies do not eliminate free radicals entirely—some are actually useful for signaling—but aim to prevent them from accumulating in ways that lead to age-related diseases. It’s like reinforcing the fortress walls of our cells, making them more resilient and less prone to collapse over time. As we refine these tools, we’ll be taking a major step toward slowing down or halting one of the principal drivers of aging. By learning to manage the chaos at the heart of our own biochemistry, we come closer to a future where old age doesn’t mean diminished function.
Chapter 4: Clearing the Cellular Junk—From Sticky Lipofuscin to Brain-Damaging Amyloids.
Our cells work hard, and like any busy place, they produce waste. Most cellular trash gets recycled efficiently, but some stubborn leftovers, known as junk, linger behind. Inside our cells, one troublemaker is lipofuscin—a complex, unwanted byproduct that builds up as we age. Cells have cleaning crews called lysosomes, responsible for breaking down waste. Yet lysosomes can’t tackle every piece of lipofuscin, leaving behind debris that clogs cellular machinery, much like uncollected garbage piling up in a town. Over time, this accumulation hinders cells’ performance, contributing to tissue damage, weaker organs, and age-related illnesses. Just as a well-run city needs effective waste management, our cells need ways to eliminate these stubborn leftovers, or we risk letting them hamper the smooth functioning of our bodies.
One imaginative idea for dealing with this junk emerged from an unusual place: graveyards. After all, human cells accumulate lipofuscin throughout life and take it with them to the grave. Since cemeteries don’t glow with the fluorescent light of this material, something in the soil must be breaking it down—likely soil microbes. These tiny decomposers can handle what our cells cannot. If we can harness these microbial enzymes and safely deliver them into our bodies, we might give our cells new tools to clear out lipofuscin. While this idea still faces technical and safety hurdles, it shows that the solutions to our aging problems might be found in unexpected corners of nature. With determination, we may transform a bizarre concept into a practical medical treatment.
Junk also lurks outside our cells. Amyloids, for instance, are harmful protein clumps that gather in spaces around neurons in our brains. As these amyloid piles grow, they interfere with brain function, making it harder for neurons to communicate and often leading to devastating conditions like Alzheimer’s disease. Our brains do have a slow, natural clean-up system, but it isn’t fast enough. Scientists propose kickstarting this removal process with a special vaccine that stimulates the brain’s immune response. By training immune cells to target and clear out amyloids more efficiently, we might halt or reverse the neurological damage they cause. Through careful development, such vaccines could become vital tools in preserving our mental sharpness far longer than is currently possible.
By ridding our cells and tissues of these various types of junk, we give ourselves a fresh start. Clearing away debris helps maintain cellular cleanliness, ensuring that our body’s delicate biochemical balance is not disrupted by accumulated clutter. It’s a bit like cleaning up an old attic—removing dusty boxes, broken furniture, and cobwebs—so you can use the space effectively again. When we combine these junk-removal strategies with mitochondrial protection and other therapies, we move closer to an era where common symptoms of aging are no longer seen as normal but as preventable damage. Proper waste management, even at a microscopic level, could help us lead longer, healthier lives, keeping our minds sharp and bodies strong deep into what we used to call old age.
Chapter 5: Tapping into the Power of Stem Cells and Taming the DNA Errors That Trigger Cancer.
One major reason we age is that our tissues gradually lose cells faster than they can be replaced. If we could restore these cells, like replenishing lost workers in a factory, we might keep our bodies youthful and robust. Stem cells, especially those sourced from early-stage embryos, hold the remarkable ability to become any type of cell we need—heart cells, brain cells, muscle cells, and more. By injecting new stem cells, or encouraging existing ones in our bodies, we could repair injured tissues or maintain organs in tip-top shape. But this powerful tool comes with ethical and moral debates. Some people worry about the source of these embryonic stem cells and question where human life truly begins, complicating this potentially life-changing solution.
Even as we dream of replenishing cell supply, we must also confront another danger of aging: cancer. Our DNA carries the instructions for building and running every cell. When DNA remains stable and undamaged, it keeps the body’s machinery humming. But as time passes, environmental factors like UV radiation and toxins, or internal factors like free radicals, can cause genetic errors. These mutations may turn healthy cells into cancerous ones that grow uncontrollably, forming tumors that threaten our lives. Because aging gives mutations more time to accumulate, it raises the likelihood of getting cancer. Thus, living longer without addressing DNA stability would mean facing an even greater cancer risk. Balancing longer life with cancer prevention is a key challenge that must be tackled thoughtfully.
One proposed solution is to eliminate the enzyme telomerase that re-lengthens the protective caps at the ends of chromosomes. These caps, called telomeres, shorten each time a cell divides. Eventually, telomeres become too short, and the cell stops dividing, which prevents potential cancer cells from multiplying endlessly. Cancer cells often reactivate telomerase, bypassing this limitation and dividing without limit. If we remove or neutralize the telomerase gene, we block cancer cells from escaping their fate. However, without telomerase, even healthy cells will age and die eventually. This is where stem cell therapy comes in. By regularly adding fresh, healthy stem cells to replace the normal cells that have reached their division limit, we might keep tissues youthful while preventing uncontrolled cancer growth.
This intricate balance—using stem cells to rejuvenate tissues while controlling telomerase to stop cancer—reflects the complexity of fighting aging at its roots. We must learn to skillfully direct our body’s cellular orchestra so that each section plays harmoniously. We can’t simply let cells live forever without control, nor can we restore tissues infinitely without protecting against rogue growths. Yet, with careful engineering, it might be possible to chart a path that allows long life with minimal cancer risk. By mastering these cellular balancing acts, we stand a chance of improving longevity and health together. This intricate dance of DNA stability, regulated cell division, and strategic cell replacement might help humanity unlock a future where aging is not an inevitable tragedy but a solvable puzzle.
Chapter 6: Battling Advanced Glycation End Products (AGEs) and Vanquishing Zombie Cells for a Healthier Body.
Have you ever noticed how certain foods turn brown or crispy when cooked? This happens due to chemical reactions that bind sugars to proteins, creating delicious flavors. Inside our bodies, a similar process occurs, producing what scientists call Advanced Glycation End Products (AGEs). Over time, AGEs gather in our tissues, making proteins stiff and less functional. This can lead to diseases, hardened arteries, and frail organs. Unfortunately, no simple prevention method exists to stop AGEs from forming. It’s as if our bodies are slowly browning from the inside, causing subtle harm that mounts with age. To counter AGEs, researchers seek drugs or special enzymes that can break them apart, restoring flexibility and health to the tissues they have quietly damaged over decades.
One candidate drug, alagebrium, showed promise in animals by breaking down certain AGEs. However, the trade-offs in humans didn’t live up to expectations. This setback doesn’t mean the end of the story. Scientists continue to test different compounds, hoping to find something that safely clears away these unwanted chemical bonds. After all, if we treat aging as a fixable problem, we must tackle the subtle factors that stiffen and weaken our tissues. With further research and innovation, we might discover better substances that undo AGE damage, letting our organs remain flexible and vital for much longer than nature currently allows.
Another hidden troublemaker are cells that refuse to die properly. When cells are damaged beyond repair, the body often pushes them into a controlled state called senescence, like switching them off so they can’t form tumors. Normally, these retired cells should quietly be removed. But sometimes they linger, leaking harmful signals that damage neighboring cells. These zombie cells don’t contribute anything useful; instead, they drag down healthy tissues. Removing or neutralizing these cells could halt a major source of age-related decline. Some strategies include selectively targeting them with suicide genes that tell them to self-destruct, or reprogramming them so they don’t become toxic in the first place. This approach is like clearing out a gang of troublemakers lurking silently in a once-peaceful neighborhood.
By defeating AGEs and zombie cells, we systematically reduce the burden of aging on our bodies. Each such victory—be it finding a perfect drug to break up AGEs or engineering a safe method to eliminate toxic cells—brings us closer to a reality where aging’s harmful effects can be kept at bay. These strategies aren’t isolated. They fit together like puzzle pieces: cleaning out cellular junk, preventing mitochondrial damage, controlling DNA mutations, and replenishing tissues. The ultimate vision is a comprehensive maintenance program for the human body, allowing us to live as though time has lost its relentless grip. While challenges remain, each small step forward in controlling these subtle threats to our health can add up to extraordinary leaps in lifespan and well-being.
Chapter 7: Proving the Concept with Mice—Robust Mouse Rejuvenation as a Testing Ground.
Ambitious ideas need proof. To convince the world that ending aging isn’t just daydreaming, scientists must show tangible results. One proposed test involves a small, unassuming creature: the common lab mouse, Mus musculus. Typically, these mice live about three years. The plan is to apply anti-aging strategies—like repairing mitochondrial DNA, clearing cellular junk, and controlling telomerase—to a group of 20 older mice. If researchers start treatments when the mice are already two years old, they begin with animals carrying plenty of age-related damage. Extending their lifespan from the usual 3 years to 5 would be a dramatic success, demonstrating that the therapies actually work, even starting late in life. This would silence many skeptics and encourage more people to support serious anti-aging research.
By targeting mice rather than humans at first, scientists can test multiple methods and adjust their approaches safely. Mice are genetically well-understood and easy to study, making them ideal pioneers on this journey. If these therapies allow older mice to become as spry, alert, and active as much younger mice, it will show that we can restore youthful function, not just increase lifespan. This would mean that we’re not simply prolonging the period of decline; we’re truly rejuvenating the body. Such visible changes would catch the public’s attention and open up more funding opportunities. In turn, this increased support would accelerate the research, pushing us closer to applying these methods to humans.
For centuries, death and aging have been considered natural enemies that no one can outsmart. If robust mouse rejuvenation succeeds, it challenges that notion. The experiment’s results may bring new respect to scientists who dedicate their lives to ending the suffering caused by age-related diseases. It will also raise new questions: If we can double a mouse’s healthy lifespan, why not a human’s? If so, what age could we reach with a fit body and a clear mind? Demonstrating success in mice is a powerful statement because it shows we have the tools to shift the boundary of what’s biologically possible. At that point, even stubborn doubters might start seeing aging as a puzzle we can solve.
Of course, some will worry about potential side effects: what if, in the process of keeping mice younger, they inadvertently trigger other issues, like an increased cancer risk or immune problems? Such concerns are valid and must be addressed. The point of these mouse experiments is not only to prove that extending healthy life is possible but to identify and refine approaches to minimize risks. By carefully analyzing results, adjusting therapies, and repeating experiments, scientists learn which methods are safest and most effective. Ultimately, robust mouse rejuvenation is just a stepping stone, a critical demonstration that aging need not be simply accepted. It paves the way for future human treatments and offers hope that we can rewrite the rules we once believed were set in stone.
Chapter 8: Balancing Risks and Rewards—Accepting Setbacks to Accelerate Human Progress.
No scientific journey is free from risk. When exploring new frontiers, occasional setbacks are inevitable. Anti-aging research may produce treatments that fail, cause unexpected harm, or even lead to tragic losses. Some individuals may argue that we should move slowly, waiting for ironclad proof before taking any bold action. They fear that untested therapies might harm people, especially when it comes to altering fundamental biological processes. However, others point out that doing nothing also comes at a cost. Countless individuals die daily from age-related conditions. Delaying potential solutions means losing more lives. Balancing these risks—being cautious but not so cautious that we halt progress—is a delicate challenge. We need ethical guidelines, transparent communication, and a willingness to learn from missteps.
History shows that medical progress is often messy. For example, in the past, a teenager tragically died during an early gene therapy trial, causing public backlash and halting research progress for months. While this caution is understandable, such slowdowns can also prevent people from accessing treatments that might save thousands of lives if they were developed sooner. It’s not about recklessness; it’s about carefully weighing the scales. How many people die while we wait for absolute certainty? How many promising ideas are abandoned because one early failure scared everyone away? To move forward, society must accept that some level of risk is unavoidable in pioneering medicine. By thoughtfully managing this risk and improving safety over time, we can still honor the value of every human life.
Some propose speeding drug approvals for anti-aging treatments once we have strong evidence in animal studies, aiming to shift the ratio of lives lost. Currently, slow approvals may cost many more lives than the rare tragedies caused by a promising but not fully tested treatment. By increasing flexibility and encouraging responsible experimentation, we might save more people who would otherwise age and die without ever receiving a potentially life-extending therapy. This does not mean being careless. It means creating a supportive environment where promising therapies can be refined and introduced more efficiently, guided by well-designed clinical trials and careful monitoring. Ultimately, smarter regulation can lead to better treatments reaching patients sooner, improving their chances of enjoying longer, healthier lives.
The goal is to transform society’s attitude toward aging from resigned acceptance to determined action. To do that, we must embrace the idea that striving for big gains often involves calculated risks. By being transparent about these challenges—showing both the failures and successes—experts can build trust with the public. When people understand that delays are not zero-risk, they might be more inclined to support informed, well-supervised trials. In time, our collective willingness to accept measured risk could push breakthroughs forward, releasing us from the stranglehold of aging. Just as we have tolerated risks in building airplanes, discovering antibiotics, or pioneering organ transplants, we must also be prepared to face uncertainties if we hope to rewrite what it means to grow old.
Chapter 9: Embracing a Future Where Aging Is Optional and Youthful Vitality Endures.
Imagine a world where seeing great-great-grandparents playing sports, exploring new careers, or discovering fresh hobbies well past their hundredth birthday becomes normal. In this vision, aging is no longer a downward spiral of pain, weakness, and disease. Instead, it’s a controlled process, managed by therapies that repair damage before it undermines our health. If we reach this point, growing older need not be synonymous with losing independence. Instead, it might simply mean accumulating more experience, wisdom, and memories, while still enjoying the energy and abilities we once thought only belonged to the young. Such a transformation would reshape our entire understanding of life, family, and society.
Some people might ask: if we stop aging, what happens to the world’s population, economies, and social structures? Would we face overcrowding, or would longer, healthier lives enable us to solve these challenges more creatively? Prolonged vitality could inspire new perspectives on education, careers, and environmental stewardship. With a century or more of robust life ahead, would people plan more carefully, treat the planet more kindly, and approach relationships and goals with renewed thoughtfulness? This future is filled with possibilities and questions. It’s an invitation to rethink everything from retirement and housing to how we define a full life.
We may one day look back at today’s acceptance of aging as a curious relic of a bygone era. Just as we marvel at how people once viewed certain diseases as unbeatable curses, future generations might shake their heads at the idea that humans ever believed aging was untouchable. When science unveils a method to maintain our bodies, minds, and cells, we can step beyond limits that once seemed carved into stone. We must remember that every major medical breakthrough—from vaccines to antibiotics—was once considered impossible or unnatural. Ending aging follows that same tradition: daring to challenge old assumptions and trusting that knowledge, empathy, and ingenuity will guide us toward a better world.
The journey isn’t easy, and it won’t happen overnight. But as research refines therapies and proves their safety, skepticism may fade. If we’ve shown that mitochondrial damage can be repaired, that cellular junk can be cleared, that cancer risks can be managed, and that tissues can be rejuvenated, then aging itself becomes a relic of our past. Picture a world where a century-old person dances, laughs, and loves like someone in their prime today. This is the promise that beckons: not an endless life of misery, but a longer, healthier, richer existence. Instead of fearing old age as an approaching storm, we could celebrate every birthday as another opportunity to live fully and contribute meaningfully to our evolving human story.
All about the Book
Explore ‘Ending Aging’ by Aubrey de Grey, a groundbreaking work that challenges conventional wisdom about aging and offers transformative insights into rejuvenation science, longevity, and the future of human health.
Aubrey de Grey is a renowned biomedical gerontologist, recognized for his pioneering research on aging and innovative approaches to extend human life, making him a leading voice in longevity science.
Gerontologists, Biomedical Researchers, Health Professionals, Philosophers, Entrepreneurs in Health Tech
Longevity Research, Health and Wellness, Scientific Literature, Biohacking, Philosophy of Aging
Biological Aging, Chronic Diseases, Healthcare Costs, Quality of Life in Old Age
The first person to live to 1, 000 years old is probably alive today.
Elon Musk, Ray Kurzweil, Peter Thiel
The Silver Innovator Award, Best Book on Longevity – 2017, James W. McKim Award for Excellence in Research
1. What if we could slow down the aging process? #2. How does cellular damage contribute to aging? #3. Can proper maintenance extend our healthy lifespan? #4. What are the key strategies for combating aging? #5. How do stem cells play a role in rejuvenation? #6. What are the seven types of aging damage? #7. Can genetic modifications enhance human longevity? #8. How do lifestyle choices impact the aging process? #9. What role do antioxidants play in aging? #10. Can we reverse aging at the cellular level? #11. How does the body repair its own damage? #12. What advancements are being made in regenerative medicine? #13. Could biotechnology hold the key to eternal youth? #14. How significant is the role of metabolism in aging? #15. What ethical dilemmas arise from life extension technologies? #16. How can community support enhance lifespan efforts? #17. What are some promising therapies targeting aging? #18. How does aging affect disease susceptibility over time? #19. In what ways can we measure biological age? #20. Can public policy influence aging research funding?
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https://www.amazon.com/Ending-Aging-Aubrey-de-Grey/dp/0452290040
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