In recent years, public and press interest in medicine to treat aging has been growing, and so more popular science and general interest articles - such as the one linked here - have been published. This is a new phase in the bootstrapping of longevity science, in which the media and the public conversation becomes more of a factor. Unfortunately people unfamiliar with the science, which means near all journalists, tend to pick random grab-bags of information for their articles and discussions. You never know just how coherent or correct or reflective of the current state of research any given piece will be, even if accurate within its narrow selection of research topics. There are a lot of differing opinions on how to proceed towards treatments for aging in the research community, and these approaches have enormously divergent expectation values: how much it will cost to get to a prototype treatment, and how many years of healthy life we can expect to gain from successful therapies. All publicity is good publicity when it comes to raising the water level for fundraising in all areas of aging research, but it matters greatly which lines of research gain greater support and funding.
This article, for example, looks only at classes of research initiative that are capable in principle of doing comparatively little for human longevity, and at great cost. The past fifteen years have demonstrated very well that is it is enormously challenging to alter human metabolism into safe new states in which aging is modestly slowed, even when we have the well-understood and well-studied example of the calorie restriction response to mimic. Billions have been spent on this, and with no result yet that is plausibly going to add more than a couple of years to human life expectancy. For that money, the research community could have completed prototypes for the full toolkit of SENS rejuvenation therapies that actually repair and remove the forms of cell and tissue damage that cause aging, not just slow down their accumulation. Repair can in principle create rejuvenation in the old, and is comparatively cheap. Slowing the pace of damage cannot do this, and is comparatively expensive. So, as I said, the type of research that prospers matters greatly.
"There is such a thing as 'biological age,' and it is distinct from chronological age," said Steve Horvath, a professor of human genetics at UCLA. "There is a huge debate about how to measure it. But everybody would agree 'biological age' should be a better predictor of how long you live than chronological age." Brian K. Kennedy, who heads the Buck Institute for Research on Aging, goes a step further. "I'm a firm believer that there is a 'biological age,' that it is different for different people, and that it can be manipulated," he said. "At least it can be manipulated in animals, and I think we will be able to manipulate it in humans, too." The idea that biological age is measurable and predictive only recently moved out of the mouse lab into human epidemiology.
A study published last year looked at roughly 1,000 New Zealanders who have been followed by researchers since their birth in the city of Dunedin in 1972 and 1973. In the Dunedin study, biological age was calculated for each person when the group was 26, 32 and 38 years old. Because the calculation was done repeatedly over a dozen years, the researchers were also able to estimate a "pace of aging" for each person. The results were startling. Even though all subjects had a chronological age of 38, their biological ages ranged from 28 to 61. There was a similarly wide range in the pace of aging. A few people showed virtually no aging over 12 years, a few showed three years of biological aging per year lived, and the rest fell in between. Cognitive and physical function tracked biological age.
A study last year found that people in their 70s whose biological age is five years greater than their chronological age have a 20 percent higher risk of dying over six years. Biological age appears to be real and able to predict the future, at least to some extent. But what is driving it? For a while it looked like the answer was: "Telomeres." The notion that telomere wear was the engine of aging had many adherents - until research revealed the story was much more complicated. "There's been 20 years of research, and the field has learned that telomere shortening plays a role in aging. But it is not the fundamental cause of aging," Horvath, the genetics professor, said. "We can debate how important it is."
A newer and more informative measure is known as the epigenetic clock. It keeps track of age-related changes in molecules, called methyl groups, that attach to the outside of our strands of DNA, like barnacles on a rope dangling off a dock. "DNA methylation" plays a part in regulating genes; its exact role is still being worked out. A person's methylation pattern is partly inherited and can be altered by lifestyle and environmental exposures. DNA damage, telomere shortening and cell senescence also change methylation patterns. But the biggest driver is the passage of time. "In my opinion, there is a fundamental aging process - the true root cause of aging," Horvath said. "We are currently designing a large human study that will test to what extent epigenetic changes underlie this process." Whatever the answer, it's clear that aging slowly, avoiding disease and living a long time are intertwined phenomena.