08 Mar Hungry for Sleep: A Role for Endocannabinoids?
Inadequate sleep, both in quality and quantity, has been associated with increased body weight and risk of obesity. Many epidemiological studies have established this link convincingly, however, such studies cannot determine causality or the direction of effect between sleep and weight. On the one hand, increased body mass index increases the risk for obstructive sleep apnoea, and thus disturbed sleep. On the other hand, experimental sleep restriction influences processes involved in energy balance and body weight regulation.
Previous studies have shown that sleep restriction leads to decreases in the satiety hormone leptin, increases in the appetite hormone ghrelin, and increases in hunger and appetite. Furthermore, recent experimental studies have demonstrated that restricted sleep results in overeating and results in increased weight gain. This raises the question why people overeat when sleep deprived.
In the latest issue of SLEEP, Hanlon and colleagues provide insights into the possible involvement of food reward mechanisms to underlie increased (unhealthy) food intake following sleep restriction. Using a randomized, crossover design, in fourteen healthy non-obese study participants on a fixed diet (three identical meals per day), they investigated the influence of restricting the sleep opportunity to 4.5 h per night (4 h 11 min of actual sleep as determined by PSG) as compared to 8.5 h per night (7 h 33 min) for 3 nights on the 24-h daily profile of hourly-sampled circulating endocannabinoids. The midpoint of the sleep opportunity was kept the same for the two conditions to limit any changes in circadian phase. Sleep restriction resulted in an increase in the peak and amplitude of the 24-h daily rhythm in circulating concentrations of a key endocannabinoid, 2-arachidonoylglycerol (2-AG) and its structural analogue 2-oleoylglycerol (2-OG), without changes in the 24-h mean. Their increase was most apparent between 2:00 pm and 9:00 pm, and the timing of their peaks was significantly delayed. Serum leptin, ghrelin, and cortisol were assessed simultaneously with the endocannabinoid rhythms. While the 24-h mean didn’t differ for any of the three hormones, sleep restriction reduced the amplitude of the 24-h leptin rhythm, advanced the timing of the first peak in ghrelin (close to bedtime), delayed the cortisol trough (close to bedtime) and advanced the cortisol peak (at scheduled awakening). The authors found a significant increase in the ratio of the peak in ghrelin and the peak in leptin, consistent with promoting hunger and appetite. Indeed, this was in agreement with an increase in hunger, in desire to eat, and in the assessment by participants of how much they would be able to eat following sleep restriction as compared to the control condition. These effects of sleep restriction were observed despite a stable BMI, similar sedentary activity, and identical meals between the conditions.
This study supports the novel insight that sleep restriction may not only lead to increased caloric intake due to changes in homeostatic regulation of energy balance, as has been shown by this group and others, but also by changes in hedonic aspects of food consumption. 2-AG is an abundant endogenous
agonist of the cannabinoid CB1 receptor widely expressed in the brain, including in reward centres, and in metabolic organs, where CB1 activation stimulates food intake and lipogenesis. Thus, the observed increase in the peak in 2-AG following sleep restriction may be part of the mechanism by which people overeat following sleep restriction.
Journal Reference:
Hanlon et al. Sleep restriction enhances the daily rhythm of circulating levels of endocannabinoid 2-arachidonoylglycerol. SLEEP 2016;39(3):653–664.
This article is comprised of material sourced from:
Commentary on Hanlon et al. Sleep restriction enhances the daily rhythm of circulating levels of endocannabinoid 2-arachidonoylglycerol.
SLEEP 2016;39(3):653–664.
Frank A.J.L. Scheer, PhD