Scientists Find Evidence That Aging Is Contagious

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Eventually, aging comes for us all — but new evidence suggests that in key ways, it may be a contagious condition.

In a provocative new study published in the journal Metabolism, scientists from South Korea and the United States found, while doing studies on human cells and with mice, that injecting the DNA messenger protein HMGB1 from an older individual can result in processes that very much look like aging.

Though it typically lives within cell nuclei and “organizes” DNA, HMGB1 gets released when its home cell starts to age or get stressed, causing the cell to stop dividing and start deteriorating in a process known as senescence. Once it’s outside of its natural habitat, the protein acts very differently, and can change forms depending on how much oxygen it’s exposed to — and when it’s lacking oxygen, HMGB1 is considered “reduced.”

Led by biomedical researchers from the Korea University College of Medicine in Seoul, the scientists behind the study found that when the protein is reduced, it seems to act as something of an “aging messenger,” causing the cells with which it binds to age and become senescent.

The oxidized form of HMGB1, on the other hand, doesn’t seem to have the same effect: when other cells were exposed to the oxidized protein, they stayed healthy and divided the way they were supposed to, the study explains.

Testing this effect out first on human kidney, lung, muscle, and skin cells, the researchers found that when exposed to the reduced form of HMGB1, healthy cells began to show signs of aging such as senescence and the release of inflammation molecules. When healthy cells were exposed to the oxidized protein, however, they continued to divide as normal and retained their health — and this effect was seen across each cell type.

Similar effects, the study notes, were seen in mouse experiments as well. When young, healthy mice were injected with small doses of reduced HMGB1, they began to show signs of premature aging within a single week, including the kind of senescence and inflammation associated with getting older.

And when they examined blood samples from adult humans between the ages of 70 and 80, the researchers found much higher levels of reduced HMGB1 as compared to people in their 40s — and the same effect was found in aged lab mice too.

“This study reveals that aging signals are not confined to individual cells, but can be systemically transmitted via the blood,” explained Ok Hee Jeon, one of the Korea University researchers who worked on the study, in a statement.

In other words, this research not only has implications for anti-aging treatments down the line, but also offers a new look at how aging appears to “move through” the body, going from cell to cell to suck out their life force like so many microscopic vampires. It’s early work, but it’s a fascinating glimpse at the mechanisms that lead us all to eventually succumb to father time.

More on aging: Women Take Peptide Injections at “Age Reversal” Event, End Up Leaving in Ambulances