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Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime Paperback – October 14, 2008

4.4 out of 5 stars 76 customer reviews

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Editorial Reviews

From the Back Cover

People alive today could live to be a thousand years old
"His clarion call to action is the message neither of a madman nor a bad man, but of a brilliant, beneficent man of goodwill, who wants only for civilization to fulfill the highest hopes he has for its future."
--Dr. Sherwin Nuland, clinical professor of surgery at Yale University School of Medicine and author of How We Die and The Art of Aging
"Seems to me this man could be put in jail with reasonable cause."
--Dr. Martin Raff, emeritus professor of biology at University College London and coauthor of Molecular Biology of the Cell
A leading researcher sketches the real "fountain of youth"
- The most realistic way to combat aging is to rejuvenate the body at the molecular and cellular level, removing accumulated damage and restoring us to a biologically younger state.  
- Comprehensive rejuvenation therapies can feasibly postpone age-related frailty and disease indefinitely, greatly extending our lives while eliminating, rather than lengthening, the period of late-life frailty and debilitation. 
- A comprehensive panel of rejuvenation therapies could probably be validated in laboratory mice within a decade.  We would then have a good chance of developing it for human use only a decade or two thereafter. 
- Removing the causes of aging-related deaths will also eliminate all the suffering that aging inflicts on most people in the last years of their lives. 
- Aging kills 100,000 people a day: old people, yes, but old people are people too.  Social concerns about the effects of defeating aging are legitimate but don't outweigh the merits of saving so many lives and alleviating so much suffering.
--This text refers to an out of print or unavailable edition of this title.

Excerpt. © Reprinted by permission. All rights reserved.

Chapter 1

It was 4 a.m. in California, but my body insisted on reminding me that it was noon in Cambridge. I was exhausted from the intercontinental flight and by a day spent in debate with some of the most influential personalities in biogerontology, at an invitation-only brainstorming workshop on ideas to combat aging. Evolutionary biologist Michael Rose was there. So were calorie restriction researchers Richard Weindruch and George Roth, nanotechnologist Robert Freitas, and several others. But I couldn’t sleep: On top of the mismatch between biological and geographical clocks, I was frustrated at what I saw as the day’s failure to make any real progress toward a concrete, realistic anti-aging plan. As I dozed and pondered, a question on the nature of metabolism and aging wormed its way into my brain and wouldn’t let go.

In my bleary irritation, I sat up, ran my hands over my beard, and began pacing the room, turning over the quandary in my mind. “Normal” metabolism was just so messy, and the raging debates in the biogerontology literature showed how difficult it was to determine what paced what: which metabolic disruptions were causes of aging, and which were effects (or secondary causes) that would simply disappear if the underlying primary causes were addressed. How could we make a positive difference in such a complex, poorly understood system? How could any meaningful change made in metabolism not be like a butterfly flapping its wings—apt to cause large, unwanted storms further down the line?

Then a second line of thought began to form in my mind—idly at first, just as a notion. The real issue, surely, was not which metabolic processes cause aging damage in the body, but the damage itself. Forty-year-olds have fewer healthy years to look forward to than twenty-year-olds because of differences in their molecular and cellular composition, not because of the mechanisms that gave rise to those differences. How far could I narrow down the field of candidate causes of aging by focusing on the molecular damage itself?

Well, I thought, it can’t hurt to make a list . . .

There are mutations in our chromosomes, of course, which cause cancer. There is glycation, the warping of proteins by glucose. There are the various kinds of junk that accumulate outside the cell (“extracellular aggregates”): beta-amyloid, the lesser-known transthyretin, and possibly other substances of the same general sort. There is also the unwholesome goo that builds up within the cell (“intracellular aggregates”), such as lipofuscin. There’s cellular senescence, the “aging” of individual cells, which puts them into a state of arrested growth and causes them to produce chemical signals dangerous to their neighbors. And there’s the depletion of the stem cell pools essential to healing and maintenance of tissue.

And of course, there are mitochondrial mutations, which seem to disrupt cellular biochemistry by increasing oxidative stress. I had for a few years felt optimistic that scientists could solve this problem by copying mitochondrial DNA from its vulnerable spot at “ground zero,” within the free-radical generating mitochondria, into the bomb shelter of the cell nucleus, where damage to DNA is vastly rarer.

Now, if only we had solutions like that for all of this other stuff, I mused, we could forget about the “butterfly effect” of interfering with basic metabolic processes, and just take the damage ITSELF out of the picture.


Well, I thought, why the bloody hell not?

I went back over my list. Protein glycation? A biotech startup was already running clinical trials using a drug that had been shown to break the dysfunctional handcuffing of the proteins that this process caused. The extracellular aggregates? Here again, animal studies had shown that you could just remove the damage, in this case by vaccinating against the amyloid plaque and letting immune cells gobble the stuff up. In theory, at least, there were all kinds of ways to deal with cellular senescence, though I wasn’t sure which of them would ultimately pan out. Anyone who’d read a newspaper in the last year knew that scientists were hotly pursuing a way to deal with the loss of cells: stem cells, cultured in the lab and delivered as a rejuvenating cellular therapy. Lipofuscin? It was at this point in my survey that I began to feel I might really be on to something, because just a year previously I’d come up with a way to eliminate lipofuscin that, although extremely novel, had already secured the enthusiastic interest of a few of the top researchers in that area. I didn’t have any radical new ideas up my sleeve for cancer; it was going to have to rely (for now, at least) on other people’s ideas. But that was okay: after all, there was already a huge effort under way to deal with it. And as for other problems arising from nuclear mutations, I had recently come to the admittedly counterintuitive conclusion that they were not in fact a major cause of age-related cellular dysfunction.

I went over my list again and again, and as I did so I became ever surer that there was no clear-cut exception. The combination of my own idea for eliminating intracellular garbage like lipofuscin; the idea I’d been championing for a few years for making mitochondrial mutations harmless; and the various other therapies being worked on by others around the world for addressing glycation, amyloid accumulation, cell loss, senescent cells and cancer—it seemed that this was really and truly an adequately exhaustive list. Not necessarily totally exhaustive—there certainly might be other things going wrong in the body—but very possibly comprehensive enough to give a few decades of extra life to people who are already in middle age before we start the treatments. And that was certainly a much more promising first step than anything that had been suggested the previous day, or in the many conferences and articles that I’d devoured over the previous few years.

For decades, my colleagues and I had been earnestly investigating aging in the same way that historians might “investigate” World War I: as an almost hopelessly complex historical tragedy about which everyone could theorize and argue, but about which nothing could fundamentally be done. Perhaps inhibited by the deeply ingrained belief that aging was “natural” and “inevitable,” biogerontologists had set themselves apart from the rest of the biomedical community by allowing themselves to be overawed by the complexity of the phenomenon that they were observing.

That night, I swept aside all that complexity, revealing a new simplicity in a complete redefinition of the problem. To intervene in aging, I realized, didn’t require a complete understanding of all the myriad interacting processes that contribute to aging damage. To design therapies, all you have to understand is aging damage itself: the molecular and cellular lesions that impair the structure and function of the body’s tissues. Once I realized that simple truth, it became clear that we are far closer to real solutions to treating aging as a biomedical problem, amenable to therapy and healing, than it might otherwise seem.

Grabbing a notepad, I jotted down the molecular and cellular changes that I could confidently list as important targets for the new class of anti-aging therapies that I would soon call SENS, the “Strategies for Engineered Negligible Senescence.” Each of them accumulated with age in the body throughout life and contributed to its pathological decay at later ages. As far as I could tell, the list was exhaustive, but I’d present it to my colleagues and see if they could add to it. I rushed downstairs before breakfast to transcribe my scrawled notes onto a flipchart in the meeting room. I was bursting to present my new synthesis to my esteemed colleagues. But truth be told, I already knew full well that at this first hearing they’d greet it with blank stares. The paradigm shift was just too great.
Copyright © 2007 by Aubrey de Grey. All rights reserved.
--This text refers to an out of print or unavailable edition of this title.

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Product Details

  • Paperback: 448 pages
  • Publisher: St. Martin's Griffin; 1 Reprint edition (October 14, 2008)
  • Language: English
  • ISBN-10: 0312367074
  • ISBN-13: 978-0312367077
  • Product Dimensions: 6.1 x 1.2 x 9.2 inches
  • Shipping Weight: 1.4 pounds (View shipping rates and policies)
  • Average Customer Review: 4.4 out of 5 stars  See all reviews (76 customer reviews)
  • Amazon Best Sellers Rank: #90,917 in Books (See Top 100 in Books)

Customer Reviews

Top Customer Reviews

Format: Hardcover
This book might be a steep read for most lay-people who aren't all that interested in cell biology or molecular chemistry, even as a passing fancy. But, the flipside of the author's depth of detail is that it allows you a glimpse into the kinds of complexities and even paradoxes that occur in the human metabolism (and how different those reactions can be even from those taking place in mice and monkeys).

DeGrey's major beef, in a nutshell, with the R&D community is that they are spending waaay too much time and energy trying to "understand" the complexities of why aging, cell damage, dysfunction, and diseases arise over time as bi-products of simply living life. He argues that we need a more targeted engineering approach -- simply FIND the damage after it has occurred, define what that damage is, and then GO FIX IT. These are much simpler problems to solve. As an analogy, look at what we do to preserve any machine or system. You can see a 100-year old house has holes in the roof; go patch them. While you're at it some new caulking around the windows, maybe some more insulation in the attic, some anti-termite spray, and there you go, good for another 100 years.

DeGrey envisions periodic therapies, say once per decade or so (similar to immunization schedules, for example) where individuals would receive viral injections and/or gene therapy to kill cancer cells, untangle proteins that cause alzheimers and the like, and remove calcification and stiffening from arteries and veins, generally restoring the body to a state of youthful vitality.

It is not nearly as "crazy as it sounds", but the fact remains that the large amounts of govt.
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Format: Paperback
So many good reviews. And being positive about this subject is great. But the book does not warrant such high reviews.

Before I get into my opinion of this, let me summarize what this book is about:

De Grey and Rae tackle the problem of aging. They view aging, primarily, as a product of junk that accumulates in the body. The junk happens because of many things: diet, our environment, mutations in our DNA, etc. But primarily because of free radical damage: oxidation. The junk deforms our tissues, both inter and intra-cellularly. It's the hostile environment of oxidation that causes the twisting of proteins in our cells, and makes them deformed and non-funcitonal.

Through the process of oxidation, like a log burning up, we basically become less and less functional as time goes on because of free radical damage. Like the log burning, we don't really have a choice if we want to keep living. Just like the log takes in oxygen to fuel its fire, so too do we take in oxygen to fuel our mitochondria that provides energy to our cells. It's that energy that keeps the cell alive, and keeps us alive. But in the process we are burning up, and dying, just like the log. Mitochondria is the culprit: the energy furnaces which exist in every cell.

In order to thwart aging, we need to clear our bodies of this junk, and reduce mutations in our mitochondria that cause them to malfunction, as well as stop hydrogen peroxide - a free radical - from being systemically released to the rest of the body. Hydrogen peroxide is a byproduct spit out by mitochondria. That is the main cause of systemic oxidation.

The solution to stopping mitochondria from oxidizing the rest of the body is to transplant it into the nucleus of the cell, shielding it.
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The basic strategy is to bootstrap: figure out how to repair the age-related damage that we know about today, and use the extra lifetime this gives us to learn how to repair the damage that will develop as we live longer and longer lives. So if you reach the age of 200, say, the damage that has to be repaired is the damage that occurs to get to 100, plus whatever becomes an additional problem between 100 and 200, and so on.

I think the basic strategy is quite sound, given the exponential progress in technology and especially bio-tech that we are seeing today. It is pretty common to hear researchers say that they can do more in a year today than they could do in 10 years previously, because the tools and our knowledge are both so much better. So once we can get to a point where we can extend current lives by 20+ years, there is a good chance that no one will die of old age ever again (except by choice).

When I talk about this, one of the immediate concerns I hear is for the planet and running out of resources. Personally, I am convinced that when this problem arrives we will solve it, and that there are a variety of ways that this could be done (much lower birth rates, higher density on this planet, moving into space and/or to other planets), so I am much more concerned with curing aging. I don't want to see any more of my friends or family die, and I would like to enjoy life as long as I want. So I am all in favor of this program!

The book is divided into three sections. One that talks about the problem of aging and treating it as an engineering problem to be solved; one that talks about the known issues that have to be solved and possible solutions; and one that talks about what each of us can do to contribute to solving the problem.
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