Why do we sleep? New discovery sheds light
Why do we sleep? Researchers at the University of Oxford in the U.K. claim to have cracked the mystery. On July 18, 2025, researchers said the physical mechanism causing drowsiness in animals appears to be an electrical overload.
That overload is in a component of brain cells – called mitochondria – that energize metabolism.
Gero Miesenböck, a co-author of the paper, described the discovery’s significance:
We set out to understand what sleep is for, and why we feel the need to sleep at all. Despite decades of research, no one had identified a clear physical trigger. Our findings show that the answer may lie in the very process that fuels our bodies: aerobic (oxygen-based) metabolism.
The need for sleep is a byproduct of how cells convert oxygen and nutrients into usable energy for the body, the research indicates. This process is the citric acid cycle. And during this process, electrons build up in mitochondria, which are a type of organelle, or subunit found in cells. Mitochondria also have the nickname of the powerhouse of the cell.
The excess electrons then “leak” into surrounding tissues. The leakage acts as a signal for the brain to initiate sleep and restore the energy imbalance. Miesenböck explained how the feedback works:
In certain sleep-regulating neurons, we discovered that mitochondria – the cell’s energy producers – leak electrons when there is an oversupply. When the leak becomes too large, these cells act like circuit breakers, tripping the system into sleep to prevent overload.
The peer-reviewed journal Nature published the findings on July 16, 2025.
Preventing cells from poisoning themselves with free radicals
Sleep also prevents tissue damage from byproducts – reactive oxygen species – that result from the leakage, said Raffaele Sarnataro, the study’s principal author:
You don’t want your mitochondria to leak too many electrons. When they do, they generate reactive molecules that damage cells.
Reactive oxygen species are a form of free radicals, and metabolism with oxygen is a primary source in the body. According to the NIH’s National Cancer Institute, free radicals are specifically linked to cancer.
Free radicals are sometimes beneficial and sometimes damaging to cells. Learning how the body mitigates damage from electrons leaking into brain tissue could also have implications for understanding aging and neurological disorders, according to other research on the topic:
Energy metabolism, oxidative stress, and sleep – three processes implicated independently in lifespan, aging and degenerative disease – are thus mechanistically connected.
The more recent publication by the team including Sarnataro and Miesenböck puts it this way:
Sleep, like aging, may be an inescapable consequence of aerobic metabolism.
Studying sleep in the lab
For their research, the investigators used fruit flies as an animal model in the lab. Besides discovering a mismatch in the number of electrons entering and exiting mitochondria as the trigger for sleep, they also learned they could control the amount of sleep the flies required. They could even put them to sleep using light:
First, opening an exit route for surplus electrons … not only relieved the basal pressure to sleep but also remedied the excessive sleep need of flies whose ability to remove breakdown products … was impaired. Second, increasing the demand … for electrons … decreased sleep. And third, powering (energy) synthesis with photons rather than electrons … precipitated sleep.
Finally, the new insights into sleep could explain why larger animals live longer than smaller ones. And these discoveries could have implications for the treatment of sleep disorders and chronic fatigue:
The findings help explain well-known links between metabolism, sleep and lifespan. Smaller animals, which consume more oxygen per gram of body weight, tend to sleep more and live shorter lives. Humans with mitochondrial diseases often experience debilitating fatigue even without exertion, now potentially explained by the same mechanism.
Bottom line: Why do we sleep? Oxford researchers may have cracked the mystery. The cause appears to be an electrical buildup in the energy-creating components in our cells, the mitochondria.
Source: Mitochondrial origins of the pressure to sleep
Read more: Parts of brain sleep, wake up, all day
The post Why do we sleep? Study blames overloaded brain cells first appeared on EarthSky.
from EarthSky https://ift.tt/Pi9Cm6f
Why do we sleep? New discovery sheds light
Why do we sleep? Researchers at the University of Oxford in the U.K. claim to have cracked the mystery. On July 18, 2025, researchers said the physical mechanism causing drowsiness in animals appears to be an electrical overload.
That overload is in a component of brain cells – called mitochondria – that energize metabolism.
Gero Miesenböck, a co-author of the paper, described the discovery’s significance:
We set out to understand what sleep is for, and why we feel the need to sleep at all. Despite decades of research, no one had identified a clear physical trigger. Our findings show that the answer may lie in the very process that fuels our bodies: aerobic (oxygen-based) metabolism.
The need for sleep is a byproduct of how cells convert oxygen and nutrients into usable energy for the body, the research indicates. This process is the citric acid cycle. And during this process, electrons build up in mitochondria, which are a type of organelle, or subunit found in cells. Mitochondria also have the nickname of the powerhouse of the cell.
The excess electrons then “leak” into surrounding tissues. The leakage acts as a signal for the brain to initiate sleep and restore the energy imbalance. Miesenböck explained how the feedback works:
In certain sleep-regulating neurons, we discovered that mitochondria – the cell’s energy producers – leak electrons when there is an oversupply. When the leak becomes too large, these cells act like circuit breakers, tripping the system into sleep to prevent overload.
The peer-reviewed journal Nature published the findings on July 16, 2025.
Preventing cells from poisoning themselves with free radicals
Sleep also prevents tissue damage from byproducts – reactive oxygen species – that result from the leakage, said Raffaele Sarnataro, the study’s principal author:
You don’t want your mitochondria to leak too many electrons. When they do, they generate reactive molecules that damage cells.
Reactive oxygen species are a form of free radicals, and metabolism with oxygen is a primary source in the body. According to the NIH’s National Cancer Institute, free radicals are specifically linked to cancer.
Free radicals are sometimes beneficial and sometimes damaging to cells. Learning how the body mitigates damage from electrons leaking into brain tissue could also have implications for understanding aging and neurological disorders, according to other research on the topic:
Energy metabolism, oxidative stress, and sleep – three processes implicated independently in lifespan, aging and degenerative disease – are thus mechanistically connected.
The more recent publication by the team including Sarnataro and Miesenböck puts it this way:
Sleep, like aging, may be an inescapable consequence of aerobic metabolism.
Studying sleep in the lab
For their research, the investigators used fruit flies as an animal model in the lab. Besides discovering a mismatch in the number of electrons entering and exiting mitochondria as the trigger for sleep, they also learned they could control the amount of sleep the flies required. They could even put them to sleep using light:
First, opening an exit route for surplus electrons … not only relieved the basal pressure to sleep but also remedied the excessive sleep need of flies whose ability to remove breakdown products … was impaired. Second, increasing the demand … for electrons … decreased sleep. And third, powering (energy) synthesis with photons rather than electrons … precipitated sleep.
Finally, the new insights into sleep could explain why larger animals live longer than smaller ones. And these discoveries could have implications for the treatment of sleep disorders and chronic fatigue:
The findings help explain well-known links between metabolism, sleep and lifespan. Smaller animals, which consume more oxygen per gram of body weight, tend to sleep more and live shorter lives. Humans with mitochondrial diseases often experience debilitating fatigue even without exertion, now potentially explained by the same mechanism.
Bottom line: Why do we sleep? Oxford researchers may have cracked the mystery. The cause appears to be an electrical buildup in the energy-creating components in our cells, the mitochondria.
Source: Mitochondrial origins of the pressure to sleep
Read more: Parts of brain sleep, wake up, all day
The post Why do we sleep? Study blames overloaded brain cells first appeared on EarthSky.
from EarthSky https://ift.tt/Pi9Cm6f
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