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Ending Pain Could Make Us Live Longer

Pain might literally be killing the elderly.
Knocking out a pain receptor could extend life. Image: Shutterstock

The more that researchers look into the science of extending life, the more they find that, often, a simple change can have extreme benefits. The latest? Knocking out a pain receptor that goes wild in older people seems to extend the lives of mice by roughly 15 percent.

Assuming an average age of 80 years or so, you're looking at a good half decade or more of high-quality life, if the results of the study can be translated to humans. A few weeks ago, scientists reported that boosting a growth factor in mice can repair brain and muscle tissue, reversing aging's effects. This latest study, published by researchers from the University of California-Berkeley in Cell, purports to prevent one of the causes of aging altogether.

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When you feel pain, the nerves in your body send signals to your brain to tell you to stop doing whatever painful thing you're doing—but, actually, the pain itself might be killing you. Mice who had their TRPV1 pain receptors genetically knocked out displayed a "youthful metabolic profile at old age," giving researchers a clue about why pain—especially in old age—might be in and of itself deadly.

"Older people report being in pain more than younger people—they say that it's because they're old," Andrew Dillin, author of the study, told me. "We turned it around the other way: Maybe they're old because they're in pain. Maybe it's pain that drives the aging process."

To be sure, there are many things that drive the aging process, but how people perceive pain could be a common one, Dillin said. As people age, they often build up something known as the CGRP molecule, which binds to the TRPV1 pain receptors. Those people are more likely to have metabolic problems later in life, which can lead to many of the signs of aging.

"Sensing pain probably has negative impacts on your lifespan, it affects how well you deal with food. If you're in pain, you won't be hungry and you won't eat," he said. "If you're not in pain, you're more free to eat and regulate your metabolism."

As I mentioned, by genetically knocking out this pain receptor, old mice's metabolisms reverted back to those of youthful mice, which allowed them to live better, and ultimately longer, lives.

Of course, pain plays an important evolutionary role; it keeps us from doing things that are going to kill us more immediately, like holding our hands on stoves or stepping on sharp items. The key, Dillin said, is figuring out how to block TRPV1 in humans without making the effect too strong. Already, some migraine-relief drugs exist to target that receptor, but they're too good for widespread use—people who take them often end up feeling no pain and burn themselves or have issues with hypothermia, Dillin told me.

Not everyone would be prescribed a TRPV1 inhibitor. Dillin says that by keeping an eye on CGRP levels, it would be easy to tell which people would stand to benefit the most from something like this.

While turning off the TRPV1 pain receptor genetically in humans will likely never be a viable way to make people live longer, developing a drug that affects it without having extreme effects might. He says that the receptor is "completely conserved in humans," so there's no reason why his mouse trial wouldn't hold the same effects in humans—the trick is just figuring out how to do it.