Anyone who has attended a class reunion has seen firsthand that people age in different ways. Some former classmates appear to have aged a century within just a few decades, while others look just as they did fresh from 11th grade English class.
Now, a study published Monday in Nature Medicine takes a deeper look at what’s going on at a molecular level, offering a possible explanation for why we age differently, and raising the tantalizing possibility that we could one day have an impact on our personal aging process through targeted medication or lifestyle changes.
Still, the research — on what a group of Stanford University scientists are calling “ageotypes” — is still in its infancy. But outside experts heralded the study as an important step toward learning more about aging.
“Exciting studies like these provide the possibility of intervening more precisely, in line with the goals of precision medicine,” said Rachel Wu, who studies aging as an assistant professor of psychology at the University of California, Riverside, and was not involved with the new study.
In the study, the researchers tracked 43 healthy adults over a two-year period, analyzing blood and other biological samples along the way to look for a variety of molecular changes.
“People are aging at different rates, but what’s equally or even more important is where you see they’re aging differently,” said study author Michael Snyder, a professor and the chair of genetics at the Stanford University School of Medicine.
That is, where in the body is the aging process most active? They found people tend to fall into one of four biological aging pathways, or ageotypes: immune, kidney, liver or metabolic.
Snyder said that metabolic agers, for example, may be at a higher risk for type 2 diabetes as they grow older. Immune agers may generate more inflammation, and therefore be at higher risk for immune-related disease. It could be that liver and kidney ageotypes may be more prone to liver or kidney diseases, respectively. There are likely other pathways, such as cardio agers who may be more prone to heart attacks, for example, but this study was limited to four main aging pathways.
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Some study participants fit multiple ageotypes, while others were found to be aging in all four categories.
“As people get older, they start to be very concerned about aging,” Snyder told NBC News. In theory, if people are able to learn their personalized ageotype, as well as the rate of their aging process, they might actively work to have an impact on it.
Wu, from UC Riverside, agreed. “It will be important to further probe how lifestyle factors may or may not interact with individual biological patterns in aging to develop more effective, tailored aging interventions across adulthood.”
“Imagine you see your [aging] slope going up a lot faster than the average group of people,” Snyder said. “Maybe that’s a kick in the pants for you to exercise more, to take the stairs more and the elevators less.” Or, perhaps, a person whose ageotype suggests rapid aging in the circulatory system might get extra imaging to look for calcium build-up in arteries.
But would such ageotype interventions translate into less disease and fewer early deaths? The science isn’t far enough along to show real-life impacts.
“That’s the missing link,” Snyder said. However, a few study participants were able to decrease or slow aging markers, at least temporarily, when they made lifestyle changes. It’s unclear what effects that could have in the long term. Other fortunate participants showed a slower-than-average aging rate throughout the study period, though researchers aren’t yet able to understand what sets those people apart from others.
Technically, people all start aging before they’re even born; every stage of development is part of the process. And many factors play roles, including genetics and the environment.
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But the research adds to the growing body of science behind not only how we age, but also why, and potential methods of intervention.
Clinical trials aimed at targeting fundamental aging processes involved in age-related diseases, such as Alzheimer’s, are already underway.
“There are drugs and various kinds of dietary interventions and lifestyle interventions through which it may be possible to modulate some of these aging processes,” said Dr. James Kirkland, a gerontologist and head of the Kogod Center on Aging at the Mayo Clinic in Rochester, Minnesota.
“But in order to apply those correctly,” he said, “we have to know which people to apply which drugs or which dietary interventions in order to get the most bang for the buck.” Kirkland was not involved with this latest study.
“It’s fine to know you’re going to get a problem based on blood tests, but you’ve got to be able to do something about it,” Kirkland added.
To be sure, there are already proven ways to reduce the risk for disease and disability: not smoking, losing extra weight, getting plenty of exercise, and a healthy diet rich in vegetables and fruit.
But, very few people accomplish all of those goals. Snyder suspects people may be more likely to make necessary lifestyle adjustments if they’re tailored to their personalized ageotype.
“I think the information could help,” he said. “It would give people motivation when they see their own increased risks.”