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.
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
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.
“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.
Prof. Snyder and his team also looked at other factors that may contribute to aging differently. More specifically, they compared the aging profiles of healthy individuals who were insulin sensitive with those of insulin resistant participants whose bodies were unable to process blood sugar effectively.
“The differences in aging between healthy and insulin resistant folks is something that’s never been looked at before,” says the senior researcher.
“Overall, we found there were about 10 molecules that significantly differed between insulin sensitive and insulin resistant folks as they aged,” he notes. Of those molecules, many played a role in the functioning of the immune system.
But the researchers also made another remarkable find: Over the 2 years during which they collected data about the participants, not everyone showed a change in ageotype markers.
Even more remarkably, for some people who changed their lifestyle — particularly in terms of diet — the ageotype markers even decreased for a time, which, in some cases, meant that these individuals were aging at a slower rate.
In some participants, age-related changes in the levels of the key molecules hemoglobin A1c and creatine, which links to kidney function, occurred at a slower rate.
Some of the individuals in whom creatine levels dropped — suggesting an improvement in kidney health — were receiving treatment with statins, the researchers explain.
In some people who made lifestyle changes, though, no improvements were obvious at the time of the study.
Prof. Snyder, who also analyzed his own biological samples over time, hopes that his lifestyle changes will prove more effective.
“I started lifting weights […],” he says, explaining that he was disappointed to see that he “was aging at a pretty average rate.” However, he thinks that his effort may pay off in the long run.
“It’ll be interesting to see if that influences my aging pathways in another year’s time,” says Prof. Snyder.
The team also notes that their current findings are just the beginning of a long and complex journey toward understanding how aging works. Many mysteries remain, and, in time, the researchers hope to uncover more answers.