Key Takeaways
- A worm study suggests obesity may impair sleep by disrupting fat-related brain signals.
- Releasing fat stores appeared to restore sleep in genetically modified worms.
- Human relevance is unclear — the findings raise questions, not clinical conclusions.
According to a new study, obesity can cause poor sleep and not the other way around, contrary to what is often assumed.
Woman in Deep Sleep
It has been repeatedly proven that poor sleep promotes weight gain. In humans, acute sleep disturbances can lead to increased appetite and insulin resistance. People who sleep less than six hours a night also have a higher risk of obesity and type 2 diabetes. However, it is not clear how sleep and diet are related. According to a new study published in PLOS Biology, it is indeed obesity that can lead to poor sleep.
“We wanted to know what sleep really does. Sleep deprivation and other chronic diseases like diabetes are related, but this is just a link. It is not clear whether not getting enough sleep is the cause of the tendency to become overweight or perhaps obesity is the cause of the tendency not to get enough sleep”, says Alexander van der Linden, associate professor of biology at the University of Nevada and co-author of the study.
To investigate the relationship between metabolism and sleep, he and his colleagues worked with microscopic worms called Caenorhabditis elegans (C. elegans) and modified a gene called KIN-29 in them to turn off a neuron that controls sleep. As a result, the worms have lost their ability to sleep. Researchers then discovered that the level of adenosine triphosphate (ATP), the body’s energy exchange currency, had significantly decreased in insomniac worms.
“This suggests that sleep is an attempt to save energy; it doesn’t actually cause energy loss,” says co-author of the study David Raizen, associate professor of neurology and a member of the Chronobiology and Sleep Institute at Penn.
Releasing the fat reserves could promote sleep
By neutralizing KIN-29 to produce worms with insomnia, the mutant worms have accumulated excess fat, similar to that found in human obesity. The release of fat reserves is therefore a mechanism that could promote sleep, researchers argue. Mutant worms may have become sleep-deprived because they cannot release fat. To test this hypothesis, the researchers manipulated the worms again, this time with an enzyme that released their fat. As a result of the fat release, the worms were able to go back to sleep.
According to the researchers, these results could partly explain why people who are obese tend to have insomnia. “There could be a signaling problem between the fat reserves and the brain cells that control sleep”, explains Raizen.
A reliable model of mammalian sleep
“Our results indicate that if you fast for a day, we assume that you might fall asleep because your energy reserves will be exhausted. – he says. In terms of sleep, there is a general feeling that sleep is a matter for the brain or nerve cells, and our work suggests that this is not necessarily true.
While these worm discoveries cannot be directly transferred to humans, C. elegans provides a reliable model for mammalian sleep, according to the scientists. In fact, like all other animals that have a nervous system, they need sleep. But unlike humans, who have complex neural circuits, C. elegans has only 302 neurons, including the sleep regulator.
So while there is still much to discover about sleep, this discovery may speed up our understanding of one of its basic functions and perhaps eventually help to treat its disorder, scientists hope.
Chronic sleep deprivation is rife in our modern societies
In general, scientists tend to see weight gain as a possible consequence of chronic sleep deprivation. For example, a 2016 English study published in the European Journal of Clinical Nutrition found that people who slept less ate an average of 385 calories more within a 24-hour period after a bad night’s sleep.
“Our results suggest that sleep is the third potential factor for weight gain, after diet and exercise,” the researchers said. Reducing sleep time is one of the most fundamental and potentially easiest factors to correct in order to lower the health risks. Chronic sleep deprivation is widespread in our modern societies, and further research is needed to assess its long-term effects on obesity and the extent to which sleep can be a preventive factor.
Bottom Line
The idea that obesity could directly disrupt sleep signals is compelling, but it’s also unproven in humans. This study shows a fat-related signaling breakdown in worms, not people, and doesn’t account for the layered causes of human insomnia, like stress, inflammation, or circadian misalignment.
The findings raise an important question: Is excess fat interfering with sleep-regulating brain circuits? But until this is confirmed in mammals, especially under real-life conditions, it remains a theory, not a shift in clinical understanding.
What’s missing here is any test of reversibility in living humans, or clarity on whether fat manipulation affects sleep independently of diet, hormones, or behavior. For now, the link between obesity and insomnia may be real, but the mechanism still isn’t.
Frequently Asked Questions
What was the main finding of the study?
Obese worms with disrupted fat signaling had trouble sleeping. Releasing stored fat helped restore sleep.
What gene did researchers modify?
They turned off the KIN-29 gene, which plays a role in fat metabolism and sleep regulation in worms.
Why did the worms lose sleep?
They couldn’t access their fat reserves, which may have prevented signals from reaching brain cells that control sleep.
Does this mean obesity causes insomnia in humans?
Not directly. The study suggests a possible mechanism, but it hasn’t been proven in people.
Can fat tissue really affect sleep?
Possibly. Some researchers believe fat may send signals to the brain about energy balance, which could influence sleep-wake cycles.
Are worms a reliable model for human sleep?
Worms are useful for studying basic biology, but their nervous systems are far simpler than ours. Results don’t always translate to humans.
What does this mean for people with obesity and insomnia?
It’s too early to say. The study highlights a possible link, but more research in humans is needed.
Could fat-releasing drugs help people sleep?
That idea is purely experimental. Nothing in this study suggests a treatment, only a biological question to explore further.
Was this peer-reviewed?
Yes. The study was published in PLOS Biology, a reputable scientific journal.
References
Grubbs, J. J., Lopes, L. E., van der Linden, A. M., & Raizen, D. M. (2020). A salt-induced kinase is required for the metabolic regulation of sleep. PLOS Biology, 18(4), e3000220. https://doi.org/10.1371/journal.pbio.3000220
