So You Want to Live Forever
Immortality through advanced technology and primitive diet
May 12, 2014, Vol. 19, No. 33 • By CHARLOTTE ALLEN
He maintains that his SENS-sponsored research, some of it conducted on the foundation’s premises and some in university laboratories, has pointed to a better way to clear that “bad” cholesterol out of clogged arteries: “We’ve been able to identify genes and enzymes in bacteria that we should be able to inject into our own human cells to bring about this cleansing process,” de Grey explained. “In 2006-2007 we succeeded in identifying some of them, and we’ve been able to have that research published. We put extra enzymes that kill bad cells into a human cell culture, and they worked. They’re the kind of microphage bacteria that we need to fix problems in the human body. Then we can work on arteriosclerosis in mice, and then we’ll have clinical trials in humans.
“The problem right now is that people think of aging as a universal phenomenon, but diseases such as heart disease are thought of as separate phenomena. But they’re universal! Ninety-nine percent of the money spent on age-related research is spent on attempts to cure those diseases. But you can’t cure people of side effects; you have to be able to cure aging itself. So what we want to see is preventative medicine, periodically cleaning up certain areas. Let’s take Alzheimer’s. We know that there are three factors: senile plaques in the brain, tangles in neurons, and cell death. We solved the plaque problem 15 years ago. You can clean up the plaques—but no cognitive goals for patients are being met. That’s because we don’t know the role that plaques play or their cause. Aging is this multifaceted. What we need to do is clean up lots of things at the same time. Initially, this could be a cleanup every 10 years. Then later, we might develop injections or oral medications. Right now, though, we have a 50-50 chance of getting it all into place in about 25 years.”
Indeed, de Grey is confident that if we can figure out how to repair just seven bodily systems prone to breakdown—ranging from chromosomal mutations over time to protein junk accumulated from the cell disintegration that accompanies aging—there is no reason for any of us to die. The only obstacle he sees to our living, say, at least 5,000 years (unless we’re unlucky enough to be hit by a car or whatever will substitute for a car in 7000 a.d.) is the money that SENS and its affiliated scientists committed to the hope of realizing eternal or near-eternal life need to develop those complex repair systems that they envision. “If we had ten times the money we have now, we could work at three times the speed,” de Grey told me.
Right now SENS, founded in 2009 by de Grey and others, has a mere $4.5 million annual budget, funded heavily from a $16 million inheritance to de Grey from his mother’s side of the family in 2011. That—coupled with the maverick nature of de Grey’s theories—undoubtedly accounts for the modest appearance of the SENS headquarters; most of the budget funds a handful of university research grants. Indeed, it took years for anyone in the world of mainstream science to take de Grey and his theories about regenerative medicine seriously.
De Grey himself looks on paper like someone hard to take seriously. A graduate of Harrow, the elite boys’ school in northwest London that Winston Churchill attended, de Grey received his bachelor’s degree in computer science from Cambridge’s Trinity Hall in 1985. His specialty was artificial intelligence. In 1990 he met and married his wife, Adelaide Carpenter, a fruit-fly geneticist at Cambridge 19 years his senior. Through his wife’s connections, he started managing a fruit-fly database part-time at Cambridge.
That was his first introduction since a biology class at Harrow to the world of biochemistry—and also to experiments on fruit-fly telomeres, the molecular caps at the ends of cells’ chromosomes that are thought to protect them from degradation. The shorter the telomere, it seems, the more prone an organism is to aging and then dying. The original length of telomeres is crucial, because as cells divide over the course of their host-organisms’ lives, telomeres’ lengths shorten substantially until they no longer offer any protection, hastening natural death, or at least the senescence that leads to death. Experiments on telomeres began during the 1970s, and more recently researchers at Harvard, using an enzyme called telomerase that inhibits telomere shortening, found that they could actually reverse the aging process in laboratory mice. Telomerase is a tricky substance for humans because it also reduces inhibitions for cancerous tumors to grow, but the discovery of its anti-aging powers has led scientists to explore the possibility of reducing cellular-level aging in other ways.
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