But this extraordinary leap in life expectancy happened without a corresponding increase in health-span. Because aging itself hasn’t been considered a medical disorder, people today generally spend half their lifetime in declining health.
Could new technologies solve these problems by extending the healthy years of long-lived populations? This is the question the emerging field of aging research has set out to answer — and labs in some of Boston’s elite institutions are among those with data suggesting that aging can be not just slowed down, but also reversed.
If we solve aging, we may well solve our emerging underpopulation crisis. (...)
In his 2019 book “Lifespan,” Harvard geneticist David Sinclair wrote that “aging may be more easily treatable than cancer.” After several years working to understand and control the biological mechanisms of aging, he tells me, his lab is showing that aging may be “like scratches on a CD that can be polished off.” His team’s latest findings were published in the journal Cell on Jan. 12. Their paper suggested mammalian aging is in part the result of a reversible loss of epigenetic information: our cells’ ability to turn genes on or off at the right time.
In “Lifespan,” Sinclair points out that if we cloned a 65-year-old person, the clone wouldn’t be born old — which says a lot about how our “youthful digital information” remains intact, even if this 65-year-old’s genetic expression and cell regulation mechanisms are presently functioning less than optimally. There seems to be, as Sinclair notes, a backup information copy within each of us, which remains retrievable.
There is no guarantee that cellular reprogramming will work in humans — but after decades of (at times, highly criticized) work, Sinclair’s lab published what is set to become a widely influential study on the role of epigenetic change in aging. Futurist Peter Diamandis, trained as a physician and now executive chairman of the XPrize Foundation (a science and technology nonprofit for which I consult), tells me aging must be “either a software or a hardware problem — solvable by a species capable of developing vaccines for a novel virus within months.”
Indeed, the human life expectancy of 80 years and the current health span of roughly 40 (when most chronic illnesses begin to appear) are not just economically alarming — they don’t appear to be a biological imperative.
Humans are one of only five species in the animal kingdom that undergo menopause. Lobsters are often more fertile at 100 than at 30. Naked mole rats’ chances of dying do not increase with age. Bowhead whales live to 200 and are incredibly resistant to the diseases of aging.
Other examples abound — and the genetic therapies that could translate these features into human bodies are becoming increasingly precise. Promising research in human genes, cells, and blood drives home that aging is a malleable process that can be decoupled from the passing of time.
It is well established that aging can be sped up, slowed down, and reversed. This is done every day with diet, mental health practices, and exercise. What’s novel about this century’s science is the promise to engineer therapies that might control the aging process more effectively.
And we have, I will suggest, an ethical imperative to do both — even though tackling aging itself as a medical problem remains a contrarian idea. (...)
Yet despite the enormous promise of aging therapies, the field hasn’t attracted a correspondingly large amount of government funding. Out of the $4 billion devoted to the National Institute of Aging yearly, only $300 million goes to fundamental aging research.
Why?
by Raiany Romanni, Boston Globe | Read more:
Image: uncredited
