What is the secret to anti-aging? It’s a question that people all over the world for thousands of years have been trying to figure out. To some, the culprit is free radicals, which are sometimes toxic molecules that our bodies produce. Not only can they incite aging, but they can also lead to heart attacks, stroke, and cancers — or so it was previously believed.
Now further information and a number of studies have substantial evidence opposing these theories. In a study published in Cell, researchers at McGill University in Canada have discovered that free radicals — by way of the mechanical makeup — tell cells when it’s time to kill themselves. They used an experimental model organism, a roundworm, to show how free radicals will promote longevity.
"People believe that free radicals are damaging and cause aging, but the so-called 'free radical theory of aging' is incorrect," says Siegfried Hekimi, a professor in McGill's Department of Biology and senior author of the study, in a press release. "We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat – not cause – aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life."
In 2010, the same researchers published a study regarding this exact theory. They also found that roundworms with genetic mutations that slowed their metabolism lived longer than regular roundworms — even though the mutated worms showed no evidence of increased protection from free radicals, Live Science reported.
This new research is important because it is "showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules," Hekimi said. "It also means that apoptosis signaling [physiological process for killing cells] can be used to stimulate mechanisms that slow down aging."
Hekimi also says that since apoptosis signaling has already been studied in great depth on people because of its links to cancer and immunity, there are also a number of pharmacological tools that scientists can use to manipulate apoptosis. He also says that Pro-longevity apoptotic signaling could open doors for more research on neurodegenerative diseases.
In the brain, the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them, he continued to explain. That's because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neuron signaling. But that doesn't mean it will be easy.
Source: Yee C, Yang W, Hekimi S. The Intrinsic Apoptosis Pathway Mediates the Pro-Longevity Response to Mitochondrial ROS in C. elegans. Cell. 2014.