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Thinking about death: High neural activity is linked to shorter lifespans

After a comprehensive study, researchers came to a startling conclusion.

The Thinker
Flickr user Todd Martin
  • Researchers have discovered that higher levels of neural activity cause shorter lifespans, with evidence drawn from studies on roundworms, mice, and humans.
  • A protein called REST appears to be a key player; REST regulates the expression of several genes, many of which affect neural activity.
  • The findings offer new targets for further studies on longevity and may even lead to the development of a longevity drug.

If there's one thing that humans can't stop thinking about, it's death. But new research published in the journal Nature suggests that all that thinking might be the very thing that brings death on.

More precisely, researchers discovered that higher neural activity has a negative effect on longevity. Neural activity refers to the constant flow of electricity and signals throughout the brain, and excessive activity could be expressed in many ways; a sudden change in mood, a facial twitch, and so on.

"An exciting future area of research will be to determine how these findings relate to such higher-order human brain functions," said professor of genetics and study co-author Bruce Yankner. While it's probably not the case that thinking a thought reduces your lifespan in the same way smoking a cigarette does, the study didn't determine whether actual thinking had an impact on lifespan — just neural activity in general.

The role of REST

To say this was an unexpected finding is an understatement. We expect that aging affects the brain, of course, but not that the brain affects aging. These results were so counterintuitive that the study took two additional years before it was published as the researchers gathered more data to convince their reviewers. Yankner was forbearing about the delay. "If you have a cat in your backyard, people believe you," he said. "If you say you have a zebra, they want more evidence."

Yankner and colleagues studied the nervous systems of a range of animals, including humans, mice, and Caenorhabditis elegans, or roundworm. What they found was that a protein called REST was the culprit behind high neural activity and faster aging.

First, they studied brain samples donated from deceased individuals aged between 60 and 100. Those that had lived longer — specifically individuals who were 85 and up — had unique gene expression profile in their brain cells. Genes related to neural excitation appeared to be underexpressed in these individuals. There was also significantly more REST protein in these cells, which made sense: REST's job is to regulate the expression of various genes, and it's also been shown to protect aging brains from diseases like dementia.

But in order to show that this wasn't simply a coincidence, Yankner and colleagues amplified the REST gene in roundworm and mice. With more REST came quieter nervous systems, and with quieter nervous systems came longer lifespans in both animal models.

A path to longevity

Neural activity in mice

Normal mice (top) had much lower levels of neural activity than mice lacking the REST protein (bottom). Neural activity is color coded, with red indicating higher levels.

Zullo et al., 2019

Higher levels of REST proteins appeared to activate a chain reaction that ultimately led to these increases in longevity. Specifically, REST suppressed the expression of genes that control for a variety of neural features related to excitation, like neurotransmitter receptors and the structure of synapses. The lower levels of activity activated a group of proteins known as forkhead transcription factors, which play a role in regulating the flow of genetic information in our cells. These transcription factors, in turn, affect a "longevity pathway" connected to signaling by the hormones insulin and insulin-like growth factor 1 (IGF1).

This longevity pathway has been identified by researchers before, often in connection with possible benefits to lifespan from fasting. Additionally, the insulin/IGF1 hormones are critical for cell metabolism and growth, features which relate to longevity in obvious ways.

The most exciting aspect of this research is that it offers targets for future research on longevity, possibly even allowing for the development of a longevity drug. For instance, anticonvulsant drugs work by suppressing the excessive neural firing that occurs during seizures, and in studies conducted on roundworms, they've also been shown to increase lifespan. This recent study shows that this connection might not be coincidental. Similarly, antidepressants that block serotonin activity have also been shown to increase lifespan. Dietary restriction has long been implicated in promoting longer lifespans as well. Dietary restriction lowers insulin/IGF1 signaling, which this study showed affects the REST protein and neural activity. More research will be needed to confirm or reject any of these possibilities, but all represent exciting new avenues to explore, possibly resulting in the extension of our lifespans.

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Quantum particles timed as they tunnel through a solid

A clever new study definitively measures how long it takes for quantum particles to pass through a barrier.

Image source: carlos castilla/Shutterstock
  • Quantum particles can tunnel through seemingly impassable barriers, popping up on the other side.
  • Quantum tunneling is not a new discovery, but there's a lot that's unknown about it.
  • By super-cooling rubidium particles, researchers use their spinning as a magnetic timer.

When it comes to weird behavior, there's nothing quite like the quantum world. On top of that world-class head scratcher entanglement, there's also quantum tunneling — the mysterious process in which particles somehow find their way through what should be impenetrable barriers.

Exactly why or even how quantum tunneling happens is unknown: Do particles just pop over to the other side instantaneously in the same way entangled particles interact? Or do they progressively tunnel through? Previous research has been conflicting.

That quantum tunneling occurs has not been a matter of debate since it was discovered in the 1920s. When IBM famously wrote their name on a nickel substrate using 35 xenon atoms, they used a scanning tunneling microscope to see what they were doing. And tunnel diodes are fast-switching semiconductors that derive their negative resistance from quantum tunneling.

Nonetheless, "Quantum tunneling is one of the most puzzling of quantum phenomena," says Aephraim Steinberg of the Quantum Information Science Program at Canadian Institute for Advanced Research in Toronto to Live Science. Speaking with Scientific American he explains, "It's as though the particle dug a tunnel under the hill and appeared on the other."

Steinberg is a co-author of a study just published in the journal Nature that presents a series of clever experiments that allowed researchers to measure the amount of time it takes tunneling particles to find their way through a barrier. "And it is fantastic that we're now able to actually study it in this way."

Frozen rubidium atoms

Image source: Viktoriia Debopre/Shutterstock/Big Think

One of the difficulties in ascertaining the time it takes for tunneling to occur is knowing precisely when it's begun and when it's finished. The authors of the new study solved this by devising a system based on particles' precession.

Subatomic particles all have magnetic qualities, and they spin, or "precess," like a top when they encounter an external magnetic field. With this in mind, the authors of the study decided to construct a barrier with a magnetic field, causing any particles passing through it to precess as they did so. They wouldn't precess before entering the field or after, so by observing and timing the duration of the particles' precession, the researchers could definitively identify the length of time it took them to tunnel through the barrier.

To construct their barrier, the scientists cooled about 8,000 rubidium atoms to a billionth of a degree above absolute zero. In this state, they form a Bose-Einstein condensate, AKA the fifth-known form of matter. When in this state, atoms slow down and can be clumped together rather than flying around independently at high speeds. (We've written before about a Bose-Einstein experiment in space.)

Using a laser, the researchers pusehd about 2,000 rubidium atoms together in a barrier about 1.3 micrometers thick, endowing it with a pseudo-magnetic field. Compared to a single rubidium atom, this is a very thick wall, comparable to a half a mile deep if you yourself were a foot thick.

With the wall prepared, a second laser nudged individual rubidium atoms toward it. Most of the atoms simply bounced off the barrier, but about 3% of them went right through as hoped. Precise measurement of their precession produced the result: It took them 0.61 milliseconds to get through.

Reactions to the study

Scientists not involved in the research find its results compelling.

"This is a beautiful experiment," according to Igor Litvinyuk of Griffith University in Australia. "Just to do it is a heroic effort." Drew Alton of Augustana University, in South Dakota tells Live Science, "The experiment is a breathtaking technical achievement."

What makes the researchers' results so exceptional is their unambiguity. Says Chad Orzel at Union College in New York, "Their experiment is ingeniously constructed to make it difficult to interpret as anything other than what they say." He calls the research, "one of the best examples you'll see of a thought experiment made real." Litvinyuk agrees: "I see no holes in this."

As for the researchers themselves, enhancements to their experimental apparatus are underway to help them learn more. "We're working on a new measurement where we make the barrier thicker," Steinberg said. In addition, there's also the interesting question of whether or not that 0.61-millisecond trip occurs at a steady rate: "It will be very interesting to see if the atoms' speed is constant or not."

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