Everyone ages differently, but why is that? A team of researchers has pinpointed four “ageotypes” — main biological pathways for aging — that could help us answer that question. Share on Pinterest The identification of four ageotypes may help explain why our bodies age in different ways. Everyone ages, but not in the same way. Getting older can often mean learning to cope with different health problems — but again, different people face different issues. Why? That is the question that a team of researchers from the Stanford University School of Medicine in California has begun to investigate in a new study. The team’s research involved a group of 43 healthy participants between the ages of 34 and 68 years who agreed to undergo assessing for molecular biology markers at least five different times over 2 years. The Stanford scientists chose this longitudinal approach to help them build detailed aging profiles to “map” individuals’ different aging parameters. “We know already there are a handful of nice molecular and clinical markers, such as high cholesterol, that are more common in older populations,” says the study’s senior author Prof. Michael Snyder. “But we want to know more about aging than what can be learned from population averages. What happens to an individual as they age? No one has ever looked at the same person in detail over time,” he explains. Prof. Snyder and his colleagues’ new study — the findings of which appear in the journal Nature Medicine — identified four different biological pathways characterizing four main types of aging. By understanding the type — or types — of aging to which a person is predisposed, it may be possible to come up with ways to delay or slow down that form of aging, the researchers argue.

Researchers find 4 ageotypes “Our study captures a much more comprehensive view of how we age by studying a broad range of molecules and taking multiple samples across years from each participant,” explains Prof. Snyder. “We’re able to see clear patterns of how individuals experience aging on a molecular level, and there’s quite a bit of difference,” he notes. The researchers analyzed a range of biological samples — including blood and stool samples — that they collected periodically from the participants. In these, they were looking for changes in the presence and activity of various microbes and telltale molecules, including proteins, metabolites, and lipids (fats). Through their analysis, the researchers pinpointed four different “ageotypes,” or aging pathways. These were: metabolic (relating to the buildup and breakdown of substances in the body), immune (relating to immune responses), hepatic (relating to liver function), and nephrotic (relating to kidney function). Prof. Snyder and his colleagues explain that people with a predisposition to metabolic aging may have a higher risk of developing conditions such as diabetes. As they age, these individuals may also have elevated levels of hemoglobin A1c, which is a measure of blood sugar levels. Yet the team also notes that people can be predisposed to not just one but two or more types of aging, thus facing a combined risk for different health problems. In addition to aging types, the team found differences in aging rates among individuals. These findings, say the researchers, have the potential to offer people more control over their lives. If we understand what form or forms of aging we are predisposed to, we are also empowered to come up with a strategy to prevent specific health problems and possibly slow down certain aging processes. “The ageotype is more than a label; it can help individuals zero in on health-risk factors and find the areas in which they’re most likely to encounter problems down the line. Most importantly, our study shows that it’s possible to change the way you age for the better.” Prof. Michael Snyder The research into aging processes is far from over, however. “We’re starting to understand how that happens with behavior, but we’ll need more participants and more measurements over time to fully flesh it out,” says Prof. Snyder.