Distracted eating can cause overconsumption. Whereas previous work has shown that cognitive load suppresses perceived taste intensity and increases subsequent consumption, the mechanism behind... Show moreDistracted eating can cause overconsumption. Whereas previous work has shown that cognitive load suppresses perceived taste intensity and increases subsequent consumption, the mechanism behind distraction-induced overconsumption remains unclear. To elucidate this, we performed two event-related fMRI experiments that examined how cognitive load affects neural responses and perceived intensity and preferred intensity, respectively, to solutions varying in sweetness. In Experiment 1 (N = 24), participants tasted weak sweet and strong sweet glucose solutions and rated their intensity while we concurrently varied cognitive load using a digit-span task. In Experiment 2 (N = 22), participants tasted five different glucose concentrations under varying cognitive load and then indicated whether they wanted to keep, decrease or increase its sweetness. Participants in Experiment 1 rated strong sweet solutions as less sweet under high compared to low cognitive load, which was accompanied by attenuated activation the right middle insula and bilateral DLPFC. Psychophysiological interaction analyses showed that cognitive load moreover altered connectivity between the middle insula and nucleus accumbens and DLPFC and middle insula while tasting strong sweet solutions. In Experiment 2, cognitive load did not affect participants’ preferred sweetness intensity. fMRI results revealed that cognitive load attenuated DLPFC activation for the strongest sweet solutions in the study. In conclusion, our behavioral and neuroimaging results suggest that cognitive load dampens the sensory processing of strong sweet solutions in particular, which may indicate higher competition for attentional resources for strong sweet than weak sweet solutions under high cognitive load. Implications for future research are discussed. Show less
Bas-Hoogendam, J.M.; Steenbergen, H. van; Tissier, R.L.M.; Wee, N.J.A. van der; Westenberg, P.M. 2020
BACKGROUND: Patients with social anxiety disorder (SAD) fear negative evaluation in social situations. Specifically, previous work indicated that social anxiety is associated with increased medial... Show moreBACKGROUND: Patients with social anxiety disorder (SAD) fear negative evaluation in social situations. Specifically, previous work indicated that social anxiety is associated with increased medial prefrontal cortex activation in response to unintentional social norm (SN) transgressions, accompanied by increased embarrassment ratings for such SN violations. Here, we used data from the multiplex, multigenerational LFLSAD (Leiden Family Lab study on Social Anxiety Disorder), which involved two generations of families genetically enriched for SAD, and investigated whether these neurobiological and behavioral correlates of unintentional SN processing are SAD endophenotypes. Of four endophenotype criteria, we examined two: first, the cosegregation of these characteristics with social anxiety (SA) within families of SAD probands (criterion 4), and second, the heritability of the candidate endophenotypes (criterion 3).METHODS: Participants (n = 110, age range 9.0-61.5 years, eight families) performed the revised Social Norm Processing Task; functional magnetic resonance imaging data and behavioral ratings related to this paradigm were used to examine whether brain activation in response to processing unintentional SN violations and ratings of embarrassment were associated with SA levels. Next, heritability of these measurements was estimated.RESULTS: As expected, voxelwise functional magnetic resonance imaging analyses revealed positive associations between SA levels and brain activation in the medial prefrontal cortex and medial temporal gyrus, superior temporal gyrus, and superior temporal sulcus, and these brain activation levels displayed moderate to moderately high heritability. Furthermore, although SA levels correlated positively with behavioral ratings of embarrassment for SN transgressions, these behavioral characteristics were not heritable.CONCLUSIONS: These results show, for the first time, that brain responses in the medial prefrontal cortex and medial temporal gyrus, superior temporal gyrus, and superior temporal sulcus, related to processing unintentional SN violations, provide a neurobiological candidate endophenotype of SAD. Show less
Jepma, M.; Verdonschot, R.G.; Steenbergen, H. van; Rombouts, S.A.R.B.; Nieuwenhuis, S. 2012
