Pedal the Cause.
Peter Adams, Ph.D., is an avid cyclist, and he loves to compete. But while he’s done his share of road races in the past, he much prefers squaring off against a different opponent: the clock.
“I’ve always gotten a lot of pleasure out of time-trialing, which is basically you against the clock,” says Adams. “It’s a huge mental and physical challenge.”
But his bike isn’t the only place where he goes head-to-head against the hands of time. A professor in the Tumor Initiation and Maintenance Program at Sanford Burnham Prebys Medical Discovery Institute, Adams is leading research into how our cells age—and how we can potentially slow that process to live longer and healthier lives.
And yes, he insists, we can slow the aging process.
“The evidence that life span and healthy aging can be controlled is overwhelming,” Adams explains. “Take the example of mice, which live two to three years, and naked mole rats, which live 25 years. That tells us that evolution has figured out a way to massively manipulate life spans.
“Beyond that, we can introduce genetic interventions in flies, worms and mice and make them live longer,” he continues. “And there are interventions such as calorie restriction that promote longevity; and exercise, which supports healthy aging.”
The cancer-aging link
As excited as Adams is about the science of aging, there was a time when it wasn’t even on his radar as a researcher.
Originally from Coventry, England, Adams started off his career studying cancer. He earned his Ph.D. at what is now Cancer Research UK, did postdoc work at Dana-Farber Cancer Institute in Boston, and spent nearly two decades at other cancer institutes, joining the Beatson Institute for Cancer Research in Glasgow, Scotland, in 2008.
But while investigating a particular gene’s role in “senescent” cells—cells that have stopped dividing—he found himself increasingly intrigued with the mechanisms of aging. Senescence is thought to prevent cancer because it stops cells from dividing uncontrollably, but there’s a downside: Senescent cells, which are inflammatory, promote aging.
At the same time, Adams was delving deeper into the epigenome—the pattern of chemical tags that turn genes “on” or “off.” But the more he studied the epigenome, the more he saw that—like senescence—the epigenome’s impact is broader than cancer. It plays a critical role in aging, too.
“It wasn’t a new discovery, but it was my own realization that there is this relationship between aging and cancer that is fascinating and poorly understood,” he explains. “Because in most cases cancer is a disease of aging. And yet we really don’t know why.”
Damage control
Eager to pursue his broader aging research in greater depth, Adams came to Sanford Burnham Prebys in December 2016, leaving his position as head of the Epigenetics Unit at Beatson and moving to San Diego with his wife, Helen, and their two daughters.
Today, his lab combines his research interests in both cancer and aging. It focuses on how chromatin (the molecular substance of a chromosome) and the epigenome change over time in ways that promote cancer and age-associated diseases.
One of his recent studies—a collaboration with Trey Ideker, Ph.D., at UC San Diego— found that interventions that extend life span made the epigenome of an old mouse look like that of a much younger one. Adams is now investigating whether epigenetic changes actually drive aging and what cellular processes cause those changes, providing possible targets for anti aging medicines. His team is also examining how inflammation is activated in senescent cells.
“The epigenome can change with age and become damaged, and these inflammatory senescent cells can be damaging,” he explains. “In a way, healthy aging is a case of damage control, through such things as proper energy utilization, food, diet and exercise.”
What is epigenetics?
Epigenetics literally means “above” or “on top of “ genetics.
Why is epigenetics important?
Whether your genes are turned “on” or “off” depends on how accessible they are. Your genes are made of DNA that coils around proteins called histones—similar to thread around a spool. Epigenetic tags on DNA and histones wrap DNA tightly or loosely, altering gene accessibility.
Both sides
Adams certainly has the exercise part of that equation covered. Each day, he cycles eight miles into work and eight miles home, often doubling the route and adding “repeats” up the Torrey Pines hill.
Cycling has been a passion since his teen years—encouraged by his dad, who gave him a red Mercian road bike for time trials for his 21st birthday. He still has that bike, and he’s passed on his love for an active lifestyle to his daughters, who are both involved in sports. The San Diego weather is perfect for sports and for Adams’ daily rides. But that’s not the reason he loves the Institute.
“Here, I have both sides of what I’m interested in,” Adams says. “It’s a great cancer institute, but there’s also this whole community of people who are really interested in the biology of aging. Everybody is very collaborative. It’s absolutely fantastic.”
Your epigenetic life
Exposure to pharmaceutical and toxic chemicals, diet, stress, exercise and other environmental factors create positive or negative epigenetic modifications with lasting effects on development, metabolism and health.
