To understand the study, you have to know a little about sleep.  There are five stages to sleep, but for simplicity’s sake, we will only discuss Rapid Eye Movement (REM or stage 5) and non-REM (stages 1-4) sleep.  All phases are important, but the most important stage of sleep is Rapid Eye Movement (REM) sleep.  You can function without REM sleep, but it is essential for learning complex tasks and may hinder your ability to perform them efficiently.  

 

REM sleep the phase of sleep in mammals associated with dreaming and characterized by random eye movement and near-complete paralysis of the body.  You may have seen this stage in a pet inch which you see their eyes appear to twitch.  They often make noises and have paw movements as they dream during REM sleep.  

 

REM sleep the phase of sleep in mammals associated with dreaming and characterized by random eye movement and near-complete paralysis of the body. You may have seen this stage in a pet inch which you see their eyes appear to twitch. They often make noises and have paw movements as they dream during REM sleep.

The medial prefrontal cortex may play a role in controlling our desire for the palatability of foods through taste, smell, and texture. People who are obese have increased activity in the prefrontal cortex when exposed to high-calorie foods. You can clearly see how the prefrontal cortex could play a role in craving and overeating.

 

One study looked at highly palatable food consumption while the prefrontal cortex becomes inactivated and REM sleep loss occurs.  As a result, the researchers discovered that inhibiting these prefrontal cortex neurons reversed the effect of REM sleep loss on sucrose consumption while having no effect on fat consumption.  Their study also found that REM sleep loss increased highly palatable food consumption compared to control animals.  However, prefrontal cortex inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption. The results suggest that the medial prefrontal cortex may play a direct role in controlling our desire to consume obesity-promoting foods such as high in sucrose content when we have reduced sleep[1].  Reduced REM sleep does not appear to affect fat consumption.  

 

One study looked at highly palatable foods (HPF) consumption while the prefrontal cortex (PFC) was inactivated and REM sleep loss was induced.  As a result, the researchers discovered that inhibiting these PFC neurons reversed the effect of REM sleep loss on sucrose consumption while having no effect on fat consumption.  Their study found that REM sleep loss increased HPF consumption compared to control animals.  However, PFC inactivation reversed the effect of REM sleep loss on sucrose consumption without affecting fat consumption.  Reduced REM sleep does not appear to affect fat consumption.  

 

Another interesting study seems to have confirmed that when sleep is restricted, levels of endocannabinoid 2-arachidonoylglycerol (2-AG) rise.  If the word endocannabinoid does not look familiar, it is a hormone that is cannabis or cannabinoid-like.  When sleep-deprived, participants reported increases in hunger and appetite concomitant with the afternoon elevation of 2-AG concentrations and were less able to inhibit the intake of palatable snacks.  Our findings suggest that activation of the endocannabinoid system may be involved in excessive food intake in a state of sleep debt and contribute to the increased risk of obesity-associated with insufficient sleep[2].

 

So what does this mean for the average person?  The findings of this study provide a link between REM sleep and overeating these highly palatable foods.  This medial portion of the prefrontal cortex may play a direct role in controlling our desire to consume weight-promoting foods, such as those high in sucrose content when we are deficient in REM sleep.  Sure if we could put an electrode in your brain and stimulate the PFC neurons, we could reverse this effect, but you already have the means to do this, and it is called sleep.