Sleep deprivation has the same effects as cannabis

Unlike cannabis, sleep deprivation has never been illegal. Yet cannabinoid receptors seem to react in the same way to both, namely to make people want to eat fatty foods. Researchers now think they know why: sleep loss affects the same neural pathways of smell as cannabis.

Sleep deprivation, a modern deficiency

It's long been known that sleep deprivation drives the search for calorie-rich foods. To decipher how this process works, Thorsten Kahnt, neurologist at the Feinberg School of Medicine of Chicago, Illinois, was inspired by studies linking sleep deprivation in humans to an increase in certain molecules in the endocannabinoid system, the receptor system notably affected by cannabis. Studies in mice have shown that this system influences odor-related brain processes, powerful appetite stimulants.

According to Thorsten Kahnt, no one had established a clear link between sleep endocannabinoid system, sleep, smell and appetite. Sleep deprivation, if it leads to the consumption of higher-calorie foods, is then associated with an increased risk of obesity, hypertension or diabetes, and could be one of the causes of the prevalence of overweight in modern societies.

To do this, he and his team asked 25 healthy volunteers to sleep either 4 or 8 hours a night. Four weeks later, the volunteers repeated the experiment, but those who slept 4 hours during the first cycle slept 8 hours and vice versa. The following evening, the volunteers provided blood samples. As expected, the sleep-deprived volunteers showed higher levels of 2-oleoylglycerol, a molecule likely to act on endocannabinoid receptors.

The privately-owned sleep reported no more hunger than their well-rested companions, and when presented with a buffet of food, both groups consumed the same average amount of calories. However, the sleep-deprived group consistently chose foods with more energy per gram, such as glazed doughnuts instead of blueberry muffins.

A question of smells

To check whether sleep affects parts of the brain treated with odors, the researchers also carried out an MRI analysis. Study participants smelled a variety of food and non-food odors, including oven roast, cinnamon buns, garlic and fir scents.

The researchers examined scans of the piriform cortex, a pear-shaped region responsible for odor interpretation in the brain and dotted with endocannabinoid receptors. If increasing the number of molecules in the endocannabinoid system altered the way the brain interpreted odor, and therefore a person's appetite, the researchers reasoned that the piriform cortex must show variations in odor-processing activity corresponding to changes in the volunteers' food preferences.

However, the researchers found that the piriform cortices of sleep-deprived participants showed increased activity in response to food-related odors, but not in a way that directly correlated with their changes in appetite. For example, two volunteers with the same increase in odor coding could have chosen foods with different amounts of fat and calories at the buffet.

This increase in olfactory activity occurs in parallel with a disturbance in the connectivity of the piriform cortex to the insula, the brain area that regulates caloric intake: people with high levels of cannabinoids have less control over how much they eat, which would explain their attraction to fattier and sweeter foods.

Kahnt points out that the causes and effects of cannabis in different brain regions are unclear. «We don't know who's talking and who's listening,» he says. But the work does reinforce the link between sleep deprivation and sensory processes. «It also highlights the role that smell plays in guiding food choices,» he says. Knowing more about how external factors can affect odor processing and appetite could lead to new approaches to treating obesity or eating disorders.