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The stomach-derived hormone ghrelin motivates food search and stimulates food consumption, with highest plasma concentrations before a meal and lowest shortly after. However, ghrelin also appears to affect the value of non-food rewards such as interaction with rat conspecifics, and monetary rewards in humans. The present pre-registered study investigated how nutritional state and ghrelin concentrations are related to the subjective and neural responses to social and non-social rewards.In a cross-over feed-and-fast design, 67 healthy volunteers (20 women) underwent functional magnetic resonance imaging (fMRI) in a hungry state and after a meal with repeated plasma ghrelin measurements. In task 1, participants received social rewards in the form of approving expert feedback, or non-social computer reward. In task 2, participants rated the pleasantness of compliments and neutral statements.Nutritional state and ghrelin concentrations did not affect the response to social reward in task 1. In contrast, ventromedial prefrontal cortical activation to non-social rewards was reduced when the meal strongly suppressed ghrelin. In task 2, fasting increased activation in the right ventral striatum during all statements, but ghrelin concentrations were neither associated with brain activation nor with experienced pleasantness. Complementary Bayesian analyses provided moderate evidence for a lack of correlation between ghrelin concentrations and behavioral and neural responses to social rewards, but moderate evidence for an association between ghrelin and non-social rewards.This suggests that ghrelin’s influence may be restricted to non-social rewards. Social rewards implemented via social recognition and affirmation may be too abstract and complex to be susceptible to ghrelin’s influence. In contrast, the non-social reward was associated with the expectation of a material object that was handed out after the experiment. This may indicate that ghrelin might be involved in anticipatory rather than consummatory phases of reward.

Two event-related brain potential (ERP) components elicited during feedback processing are the frontocentral feedback-related negativity (FRN), followed by the posterior P300. According to the Error-Related Reinforcement Learning Theory (Holroyd & Coles, 2002), the FRN amplitude is largest when the outcome is negative and unexpected. Complementing this, studies on the subsequent P300 have often reported larger amplitudes for positive than negative outcomes. In an influential ERP study, Hajcak et al., (2005) manipulated outcome valence and expectancy in a guessing task. However, they found that the FRN component was larger for negative (no-reward) than positive (reward) outcomes, irrespective of expectancy. Conversely, the P300 component was larger for unexpected than expected outcomes, irrespective of valence. These results were at odds with prominent theories and extant literature. Here, we aim to replicate these results within the #EEGManyLabs project (Pavlov et al., 2021). Across thirteen labs we will not only undertake a close replication, but test the robustness of these effects to analytical choices (e.g. quantification of ERPs) and supplement the findings with Bayesian multilevel linear models to test for the reported absence of the effects.

Energy deprivation as well as hormones that regulate appetite and eating can influence olfactory function. This study investigated olfactory sensitivity for a food-related and a non-food odour prior to and after a meal, and its relationship to the energy-regulating hormones ghrelin and adiponectin.The olfactory sensitivity for orange and rose (PEA) odour in healthy, normal-weight volunteers (19 women, 45 men, 1 undisclosed individual) was not affected by the consumption of a meal. Olfactory sensitivity was not associated with concentrations of circulating ghrelin. However, olfactory sensitivity was higher for women than for men, indicating better olfactory performance. This difference between women and men was related to concentrations of plasma adiponectin, an adipose-specific hormone.Adiponectin may thus explain why sex differences in olfactory sensitivity emerge, and may also account for some of the inconsistencies in previous findings on sex differences. Our findings add to the limited literature on the impact of stomach and adipose tissue-derived hormones on olfactory sensitivity. Further studies are needed to establish a causal link between circulating adiponectin and a sex difference in olfactory sensitivity.