A growing body of research has shown the link between obesity and sleep loss. However, it was unclear the “chicken and egg” relationship between the two – does sleep loss result in weight gain, or does weight gain lead to poor sleep quality?
A study in PLOS Biology suggested that it is not the sleep loss that leads to obesity, but rather that excess weight can cause poor sleep, according to researchers from the University of Pennsylvania’s Perelman School of Medicine and the University of Nevada, Reno.
Sleep is a function of the body trying to conserve energy when energetic levels are going down. For example, you were to fast for a day, you might get sleepy because your energetic stores would be depleted.
In humans, acute sleep disruption are known to cause in increased appetite and insulin resistance. It is noted that people who chronically get fewer than six hours of sleep per night are more likely be obese and diabetic. Moreover, starvation in humans has been shown to affect sleep, indicating that sleep is regulated, at least in part, by nutrient availability.
However, the mechanism how sleeping and eating correlate has remained unclear. Scientists have known for a while that short sleep are linked to chronic conditions such as diabetes. However, it’s not clear if short sleep is causing the propensity for obesity, or that the obesity, perhaps, causes the propensity for short sleep.
To study the association between metabolism and sleep, the researchers genetically modified C. elegans to “turn off” a neuron that controls sleep. These worms could still eat, breathe, and reproduce, but they lost their ability to sleep. With this neuron turned off, the researchers saw a severe drop in adenosine triphosphate (ATP) levels, which is the body’s energy currency. This suggests that sleep is a biological attempt to conserve energy; it’s not actually causing the loss of energy.
In previous research, another lab studied a gene in C. elegans called KIN-29. This gene is homologous to the Salt-Inducible Kinase (SIK-3) gene in humans, which was known to signal sleep pressure. Surprisingly, when the researchers knocked out the KIN-29 gene to create sleepless worms, the mutant C. elegans accumulated excess fat — resembling the human obesity condition — even though their ATP levels lowered.
The researchers hypothesized that the sleep is promoted by release of fat storage, and that the reason KIN-29 mutants did not sleep is because they were unable to liberate their fat. To test this hypothesis, the researchers again manipulated the KIN-29 mutant worms, this time expressing an enzyme that “freed” their fat. With that manipulation, the worms were again able to sleep.
The same mechanism may explain why people with obesity may experience sleep problems. There could be a signaling problem between the fat storage and the brain cells that control sleep.
What’s the take home message from this research? Obesity and poor sleep quality form a vicious cycle – obesity causes poor sleep quality, which leads to additional weight gain. Losing weight might help to improve your sleep quality and get your body into a positive cycle.
Thanks for reading.
Journal Reference: Jeremy J. Grubbs, Lindsey E. Lopes, Alexander M. van der Linden, David M. Raizen. A salt-induced kinase is required for the metabolic regulation of sleep. PLOS Biology, 2020; 18 (4): e3000220 DOI: 10.1371/journal.pbio.3000220