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Schmid, S. M.

Publications and source records attributed to Schmid, S. M..

2 recordsLinked to original sources

Eating to dare - Nutrition impacts human risk decision and related brain function

Macronutrient composition modulates plasma amino acids that are precursors of neurotransmitters and can impact brain function and decisions. Neurotransmitter serotonin has been shown to regulate not only food intake, but also economic decisions. We investigated whether an acute nutrition-manipulation inducing plasma tryptophan fluctuation affects brain function, thereby affecting risky decisions. Breakfasts differing in carbohydrate/protein ratios were offered to test changes in risky decision making while metabolic and neural dynamics were tracked. We identified that a high-carbohydrate/protein meal increased plasma tryptophan which mapped to individual risk propensity changes. Moreover, the meal-driven fluctuation in tryptophan and risk propensity changes were modulated by individual difference in body fat mass. Using fMRI, we further identified activation in the parietal lobule during risk-processing, of which activities 1) were correlated with the risk propensity changes in decision making, 2) were sensitive to the tryptophan fluctuation, and 3) were modulated by individuals body fat mass. Furthermore, the activity in the parietal lobule positively mediated the tryptophan-fluctuation to risk-propensity-changes relationship. Our results provide evidence for a personalized nutrition-driven modulation on human risky decisions and its metabolic and neural mechanisms.

neuroscience↗

Sleep deprivation selectively up-regulates an amygdala-hypothalamic circuit involved in food reward

Sleep loss is associated with increased obesity risk, as demonstrated by correlations between sleep duration and change in body mass index or body fat percentage. Whereas previous studies linked this weight gain to disturbed endocrine parameters after sleep deprivation (SD) or restriction, neuroimaging studies revealed up-regulated neural processing of food rewards after sleep loss in reward-processing areas such as the anterior cingulate cortex, ventral striatum and insula. To tackle this ongoing debate between homeostatic versus hedonic factors underlying sleep loss-associated weight gain, we rigorously tested the association between SD and food cue processing using high-resolution fMRI and assessment of hormones. After taking blood samples from thirty-two lean, healthy men, they underwent fMRI while performing a neuroeconomic, value-based decision making task with snack food and trinket rewards following a full night of habitual sleep (HS) and a night of SD in a repeated-measures cross-over design. We found that des-acyl ghrelin concentrations were increased after SD compared with HS. Despite similar hunger ratings due to fasting in both conditions, participants were willing to spend more money on food items only after SD. Furthermore, fMRI data paralleled this behavioral finding, revealing a food reward-specific up-regulation of hypothalamic valuation signals and amygdala-hypothalamic coupling after a single night of SD. Behavioral and fMRI results were not significantly correlated with changes in acyl, des-acyl or total ghrelin concentrations. Our results indicate that increased food valuation after sleep loss is due to hedonic rather than hormonal mechanisms.

neuroscience↗