Why Our Understanding of How Obesity Affects Sleep May Be Wrong

The link between obesity and sleep has been known for some time now, with studies having shown that people with obesity suffer from poor sleep. The prevailing thought has been that insufficient or poor sleep quality can lead to weight gain; however, new research now shows that the reverse directionality of the association may be true – that obesity may lead to poor sleep.

In a recent paper published in the journal PLOS Biology, researchers from the University of Pennsylvania’s Perelman School of Medicine and the University of Nevada, Reno reported that elevated metabolic energy stores, in the form of excess fat, can negatively influence sleep.

Metabolism is closely connected to sleep, with acute sleep loss shown to increase appetite and insulin resistance, while chronic sleep issues may lead to obesity and diabetes. Moreover, it has been shown that starvation in humans, rats, Drosophila and C. elegans positively affects sleep, demonstrating a link between sleep and nutrient availability.

“We think that sleep is a function of the body trying to conserve energy in a setting where energetic levels are going down. Our findings suggest that if you were to fast for a day, we would predict you might get sleepy because your energetic stores would be depleted,” said co-author of the study, Dr. David Raizen, associate professor of neurology and member of the Chronobiology and Sleep Institute at Penn State.

Related: Study: Excess Sugar Intake Could Increase Risk of Death Regardless of Weight

The researchers on the study examined sleep patterns in the microscopic worm C. elegans. They found that the tyrosine kinase KIN-29, the C. elegans homolog of a mammalian Salt-Inducible Kinase (SIK) that regulates sleep and metabolism, is involved in the link between ATP levels and sleep in the worms.

The study showed that worms that had a mutation in the kin-29 gene exhibited reduced ATP levels, exhibited starvation behavior despite having high fat stores (indicating a defective response to cellular energy levels) and also had sleep defects. Mobilization of triglycerides from fat stores was found to restore sleep, demonstrating a link between energy homeostasis and sleep.

In addition, the study found that KIN-29 interacts with HDA-4, a class IIa histone-deacetylase that regulates gene expression, in sensory neurons involved in energy homeostasis. These neurons are shown to interact with the sleep-promoting interneurons ALA and RIS. Together, these neurons form an interconnected network in which metabolic energy status is linked to sleep mechanics.

The study concluded that, “These results indicate that sleep is regulated via hierarchical interactions between neurons that sense energy needs, fat-storage cells that respond to energy need, and the action of sleep-inducing.”

Dr. Raizen explained that while these findings in worms may not translate directly to humans, C. elegans is a fairly good model for studying mammalian sleep patterns as both have nervous systems that regulate sleep. However, unlike humans, they have a much simpler nervous system, comprised of only 302 neurons, one of which regulates sleep, making it easier to study.

By gaining further understanding of how sleep is regulated, these findings may help uncover ways to treat sleep disorders.

“There is a common, over-arching sentiment in the sleep field that sleep is all about the brain, or the nerve cells, and our work suggests that this isn’t necessarily true,” said Dr. Raizen. “There is some complex interaction between the brain and the rest of the body that connects to sleep regulation.”