Sunday, April 2, 2017

Sunday Long Read: The Technology Of Immortality

This week's Sunday Long Read is New Yorker author Tad Friend's piece on Silicon Valley's quest to find the fountain of youth: clinical immortality and the end of aging.  Nobody it seems is more interested in finding the keys to controlling human lifespan more than the young titans of tech, who want to be around to see -- and to direct -- human development long, long into our future.

For decades, the solution to aging has seemed merely decades away. In the early nineties, research on C. elegans, a tiny nematode worm that resembles a fleck of lint, showed that a single gene mutation extended its life, and that another mutation blocked that extension. The idea that age could be manipulated by twiddling a few control knobs ignited a research boom, and soon various clinical indignities had increased the worm’s life span by a factor of ten and those of lab mice by a factor of two. The scientific consensus transformed. Age went from being a final stage (a Time cover from 1958: “Growing Old Usefully”) and a social issue (Time, 1970: “Growing Old in America: The Unwanted Generation”) to something avoidable (1996: “Forever Young”) or at least vastly deferrable (2015: “This Baby Could Live to Be 142 Years Old”). Death would no longer be a metaphysical problem, merely a technical one.

The celebration was premature. Gordon Lithgow, a leading C. elegans researcher, told me, “At the beginning, we thought it would be simple—a clock!—but we’ve now found about five hundred and fifty genes in the worm that modulate life span. And I suspect that half of the twenty thousand genes in the worm’s genome are somehow involved.” That’s for a worm with only nine hundred and fifty-nine cells. The code book is far more complex for animals that excite our envy: the bee larva fed copiously on royal jelly that changes into an ageless queen; the Greenland shark that lives five hundred years and doesn’t get cancer; even the humble quahog clam, the kind used for chowder, which holds the record at five hundred and seven.

For us, aging is the creeping and then catastrophic dysfunction of everything, all at once. Our mitochondria sputter, our endocrine system sags, our DNA snaps. Our sight and hearing and strength diminish, our arteries clog, our brains fog, and we falter, seize, and fail. Every research breakthrough, every announcement of a master key that we can turn to reverse all that, has been followed by setbacks and confusion. A few years ago, there was great excitement about telomeres, Liz Blackburn’s specialty—DNA buffers that protect the ends of chromosomes just as plastic tips protect the ends of shoelaces. As we age, our telomeres become shorter, and, when these shields go, cells stop dividing. (As Blackburn said, “It puts cells into a terribly alarmed state!”) If we could extend the telomeres, the thinking went, we might reverse aging. But it turns out that animals with long telomeres, such as lab mice, don’t necessarily have long lives—and that telomerase, the enzyme that promotes telomere growth, is also activated in the vast majority of cancer cells. The more we know about the body, the more we realize how little we know.

Still, researchers plunge ahead. Understanding isn’t a precondition for successful intervention, they point out; we had no real grasp of virology or immunology when we began vaccinating people against smallpox.

In the murk of scientific inquiry, every researcher looks to a ruling metaphor for guidance. Aubrey de Grey likes to compare the body to a car: a mechanic can fix an engine without necessarily understanding the physics of combustion, and assiduously restored antique cars run just fine. De Grey is the chief science officer of Silicon Valley’s sens Research Foundation, which stands for Strategies for Engineered Negligible Senescence—a fancy way of saying “Planning Your Comprehensive Tune-up.” An Englishman who began his career with a decade of work in A.I., he speaks with rapid fluidity, often while stroking his Rasputin-length beard. De Grey has proposed that if we fix seven types of physical damage we will be on the path to living for more than a thousand years (assuming we can avoid getting hit by a bus or an asteroid).

When I met him at the sens office, in Mountain View, he told me, “Gerontologists have been led massively astray by looking for a root cause to aging, when it’s actually that everything falls apart at the same time, because all our systems are interrelated. So we have to divide and conquer.” We just need to restore tissue suppleness, replace cells that have stopped dividing and remove those that have grown toxic, avert the consequences of DNA mutations, and mop up the gunky by-products of all of the above. If we can disarm these killers, de Grey suggests, we should gain thirty years of healthy life, and during that period we’ll make enough further advances that we’ll begin growing biologically younger. We’ll achieve “longevity escape velocity.”

De Grey vexes many in the life-extension community, and one reason may be his intemperate life style. He told me, “I can drink as much as I like and it has no effect. I don’t even need to exercise, I’m so well optimized.” Until recently, he maintained two girlfriends and a wife. Now, he said, “I’m engaged, and my polyamorous days are behind me.”

But the main reason is his prophetic air of certainty. His 2007 book, “Ending Aging,” is replete with both exacting research into the obstacles to living longer and proposed solutions so ambitious that they resemble science fiction. De Grey’s fix for mitochondrial mutation, for instance, is to smuggle backup copies of DNA from the mitochondria into the vault of the nucleus, which evolution annoyingly failed to do—probably because the proteins needed in the mitochondria would ball up during their journey through the watery cell body. His fix for that, moving the DNA one way and the proteins that it produces another, amounts to a kind of subcellular hokey pokey. A number of scientists praise de Grey for anatomizing the primary threats, yet they see troubleshooting all seven pathways through such schemes—and you have to troubleshoot them all for his plan to work—as a foredoomed labor. Matt Kaeberlein, a biogerontologist at the University of Washington, said, “It’s like saying, ‘All we have to do to travel to another solar system is these seven things: first, accelerate your rocket to three-quarters of the speed of light . . . ’ ”

The great majority of longevity scientists are healthspanners, not immortalists. They want to give us a healthier life followed by “compressed morbidity”—a quick and painless death. These scientists focus on the time line: since 1900, the human life span has increased by thirty years—and so, as a consequence, have cancer, heart disease, stroke, diabetes, and dementia. Aging is the leading precondition for so many diseases that “aging” and “disease” are essentially metonyms. Accidents and violence are the leading causes of death up to age forty-four, then cancer rises to the top, and then, at sixty-five, heart disease. Healthspanners want to understand the etiologies of cancer and heart disease and then block them. Why do we almost never get those diseases at age two? How can we extend that protection to a hundred and two? But if we cured cancer we would add only 3.3 years to an average life; solving heart disease gets us an extra four. If we eliminated all disease, the average life span might extend into the nineties. To live longer, we’d have to slow aging itself.

Conquering both genetic diseases and stopping the aging clock will be the big medical goal of the 21st century.  Of course, solving that riddle will only lead to a host of other issues to be tackled, the most pressing being where do you put billions of humans who do not age when we're already doing a great job of wrecking the only planet we currently have.  Still, the titans of tech see this as another problem they have the unique capability of solving.  Maybe they're right.


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