Post by Shireen Parimoo

What's the science?

Sleep deprivation is linked to weight gain, and this is largely attributed to hormones like ghrelin and leptin, which are involved in promoting and inhibiting hunger, respectively. Other studies suggest that this link is due to altered activity in brain regions associated with food reward processing following sleep deprivation, like the hypothalamus. It is currently unclear whether endocrine factors or reward-processing regions of the brain have a greater impact on food valuation following sleep deprivation, or whether they interact to affect food valuation. This week in the Journal of Neuroscience, Rihm and colleagues explored the role of endocrine function and reward processing in the brain to understand the relationship between sleep deprivation and food valuation.

How did they do it?

Thirty-two healthy young male participants completed the Becker-deGroot-Marschak (BDM) auction task in two sessions; one following habitual sleep and one following a night of sleep deprivation. In the sleep deprivation condition, participants remained awake all night and did not eat anything. The BDM task consists of three phases and provides a measure of participants’ valuation of food and non-food items. In the first bidding phase, participants were shown food and non-food items and asked how much they would spend on the items (subjective value), with a maximum limit of 3 €. For each participant, the median price across all items was used as a reference price for the choice phase. In the choice phase, participants were presented with the same items while they underwent functional magnetic resonance imaging (fMRI) scanning and asked if they would purchase each item for the reference price. Finally, in the post-scan auction, one food and one non-food item were selected at random from the first and the second phase, and the participants’ bid competed against a computer-generated price to determine if they won the item.

The authors assessed participants’ willingness to pay for the items and the probability that they would buy a given item during the choice phase of the BDM task in each session. They also collected blood samples in order to measure ghrelin (total ghrelin, acyl ghrelin and des-acyl ghrelin), leptin, cortisol, insulin, and glucose. Finally, they examined changes in the activation and functional connectivity of brain regions involved in food and reward processing across the habitual sleep and sleep deprivation conditions.

What did they find?

Sleep deprivation influenced participants’ valuation of food rewards. Participants were more willing to pay for food following sleep deprivation than after a night of sleep, but there was no difference in their valuation of non-food items. All participants in both conditions combined were more likely to buy food items than non-food items. The change in subjective value of items across the two sessions was positively correlated with the change in the probability that the participant would buy the food items. That is, if participants indicated that they would spend more money on food items in the bidding phase following sleep deprivation, they were also more likely to purchase food items during the corresponding choice phase. The concentration of des-acyl ghrelin was higher following sleep deprivation, but this did not correlate with food valuation. Brain activity on the other hand, was correlated with food valuation. Following sleep deprivation, there was greater activation of the hypothalamus for food rewards with higher subjective value. Similarly, the right amygdala was more active for food items than for non-food items after sleep deprivation. Functional connectivity analyses revealed that during the choice phase of the BDM task, activity in the right amygdala was coupled with activity in the bilateral hypothalami and the left orbitofrontal cortex, but activity in the hypothalamus was not coupled with other brain regions. This indicates that changes in food valuation following sleep deprivation are associated with activation of brain regions involved in food reward processing but not hormone concentrations, and that the altered neural activity was not driven by changes in endocrine function.