As Tolstoy wrote in Anna Karenina, “All happy families are alike; each unhappy family is unhappy in its own way.” The same can be said about how we age. We all may start out relatively healthy, but as time passes, different things start to break down inside different people, and the result is our very own unique aging journey. According to a comprehensive new study published in Science, the individuality of aging is especially conspicuous at the molecular level.
For eight years, an international team of scientists led by researchers at King’s College London followed a group of 335 healthy women from the U.K.. During that time, the team took blood samples to measure expression changes in 16,000 genes as well as the levels of hundreds of metabolites. The results were some of the most detailed long-term studies of transcriptomics and metabolomics related to aging to date.
Read more: “How Our Perceptions of Aging Can Affect Our Social Lives”
While most of their findings involved gene expression, one nugget from the metabolome stood out. Levels of forever chemicals like polyfluoroalkyl substances (PFAS) actually declined in the cohort over time. According to the team, this is “consistent with the introduction of regulations limiting the use of PFAS in the United Kingdom.” In other words, you could see the impact from restricting PFAS in the blood of the cohort, which is pretty remarkable.
Okay, on to the genetics. The researchers found that some genes showed clear trends for almost everyone. Expression of the gene for the tumor-suppressor gene p53, for example, decreased over time in the cohort. This protein, also known as the “guardian of the genome,” prevents genetic mutation (and tends to be defunct in most cancer cells).
The team also found our immune systems undergo a sort of remodeling as we age, rather than a steady decline. Generally speaking, as we get older our immune systems shift from relying on adaptive immunity (T-cells and B-cells quickly identifying and surgically eliminating new threats) toward innate immunity (a slower, always-on alert system indiscriminately taking out foreign invaders).
The researchers found that genes associated with T-cells, adaptive immunity assassins, were downregulated, while genes associated with natural killer cells, the wandering ronins of the innate immune system, were upregulated. This shift in immune system gene expression is commensurate with inflammaging, or the low-grade increase in inflammation that occurs as we age.
But most interesting were the individual peculiarities in gene regulation they discovered. Some genetic sequences, the researchers found, showed wildly different expression patterns from person to person, both in direction and intensity. One of these genes, CXCL9, is involved in cardiac aging and also happens to be the single strongest contributor to an inflammatory aging clock. And some individuals even showed breaks from the broader trends (like downregulation of p53) that were either attenuated or in the opposite direction.
“Rather than there being a single molecular road map of aging, our study shows that people follow distinct biological journeys,” study author Julia El-Sayed Moustafa of King’s College explained in a statement. “Two healthy people of the same age can be aging in surprisingly different ways at the molecular level.”
It’s a finding that could pave the way for more personalized treatments in the future. Until then, just remember there are plenty of roads that lead to healthy aging.
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