Westcott may be on to something. She’s a participant in the New England Centenarian Study, a long-term research project at the Boston Medical Center that studies why people like her enjoy such exceptional longevity. What they’ve found, thus far, is that healthy habits and positive attitudes will only get you so far: Centenarians are winners of the genetic lottery and, like Westcott, have a clustering of long-lived relatives. They are remarkably intact mentally, and up to 90 percent of them can function independently into their ninth decade. Surviving past age 100 means they’ve largely evaded the scourges that kill their peers before they reach their 90s (what’s called compressed morbidity), or sidestepped the worst aspects of these life-threatening diseases — even if they strike sooner — because they have combinations of protective genes, what researchers call “greater functional reserves.”
“Even though they have these illnesses, they handle them better than other people and have better protective mechanisms,” says Thomas Perls, a geriatrician at Boston University and director of the New England Centenarian Study. “In other words, the older you get, the healthier you have been.”
Now scientists like Perls are sifting through millions of DNA markers to spot the constellation of longevity genes that’s carried in every cell of these centenarians’ bodies. Perls and his colleagues have uncovered 281 genetic markers that seem to perform a protective function, slowing aging and making this group less vulnerable to disease. Other researchers, in sequencing the genome of centenarians, have found they possess fewer of the genes that contribute to major diseases. “They live longer, in part, because they don’t get sick,” says Stuart Kim, one of the study co-authors and a geneticist at Stanford University.
How does this happen? Scientists suspect there may be some kind of intrinsic biological clock that runs slower in some people and quicker in others, which would accelerate aging and wear down the body’s protective processes. Those with faster clocks are then more vulnerable to the onset of fatal diseases and die sooner. Research into the genetics of long-livers, and into other biological systems that may influence aging, offers some tantalizing clues into the underlying mechanics of these clocks. Deciphering precisely how they work could enable us to tinker with these internal timepieces and genuinely slow down the aging process.
Timing seems to be a key piece of the puzzle. Biological age doesn’t always match what’s on a person’s birth certificate. After all, we’re not surprised to see a 70-something debilitated by illness, or a 74-year-old who barnstorms around the country, running for president. Some people simply age faster than others, and scientists are beginning to understand why. New research using data from a landmark longitudinal study has been particularly eye opening. Known as the Dunedin study, it followed more than 1,000 people from their births in the early 1970s in the same hospital in southern New Zealand.
“Clearly, there are basic molecular mechanisms of aging that cause the various diseases that disable and ultimately kill us.”
Most research looks at aging in older people, but the seeds of age-related diseases are planted decades earlier — that’s why these researchers believe it’s crucial to study aging in the young. They aim to shed light on why we become vulnerable to the assaults of time and the chronic diseases linked to aging, such as cancer, heart disease, diabetes, and loss of mental acuity. Scientists in the U.S., U.K., Israel and New Zealand looking at the Dunedin data used it to track 18 biological measures, including liver and kidney function, blood sugar and cholesterol levels, balance, cognitive ability, cardiovascular fitness and even gum recession in 954 study participants.
As expected, most people’s biological age clustered around their early 40s, within a few years of their actual ages, according to results released last year. But there were wide variations: A handful were up to a decade younger, while many had a biological age in their 50s; one participant had a biological age of 61. Even before midlife, some participants were aging much faster. They were already having trouble with climbing stairs and difficulties solving unfamiliar mental tasks, their balance was worse, their livers were starting to fail, and they were in poorer overall health.
“When we assembled all the data, we were quite struck about the coordinated changes we did see in all the systems of the body,” says Daniel Belsky, the study’s lead author and a gerontologist at Duke University’s Center for Aging. “Clearly, there are basic molecular mechanisms of aging that cause the various diseases that disable and ultimately kill us.”
The Cellular Counter
More than 50 years ago, a researcher uncovered the first clues that an internal biological clock might regulate age — and that it’s not just the daily assaults from the external wear and tear of life that cause us to wither and eventually die. That’s when Leonard Hayflick discovered what would become known as the Hayflick limit. In the late 1950s, as a young microbiologist at the Wistar Institute in Philadelphia, Hayflick studied viruses that might cause cancer. While there, he worked with cell cultures derived from human fetal tissue. One day, the cell division in one of the flasks seemed to be slowing down, and after about the 40th doubling, the cells stopped reproducing.