Metabolic state alters economic decision making under risk in humans

Background: Animals' attitudes to risk are profoundly influenced by metabolic state (hunger and baseline energy stores). Specifically, animals often express a preference for risky (more variable) food sources when below a metabolic reference point (hungry), and safe (less variable) food sources when sated. Circulating hormones report the status of energy reserves and acute nutrient intake to widespread targets in the central nervous system that regulate feeding behaviour, including brain regions strongly implicated in risk and reward based decision-making in humans. Despite this, physiological influences per se have not been considered previously to influence economic decisions in humans. We hypothesised that baseline metabolic reserves and alterations in metabolic state would systematically modulate decision-making and financial risk-taking in humans. Methodology/Principal Findings: We used a controlled feeding manipulation and assayed decision-making preferences across different metabolic states following a meal. To elicit risk-preference, we presented a sequence of 200 paired lotteries, subjects' task being to select their preferred option from each pair. We also measured prandial suppression of circulating acyl-ghrelin (a centrally-acting orexigenic hormone signalling acute nutrient intake), and circulating leptin levels (providing an assay of energy reserves). We show both immediate and delayed effects on risky decision-making following a meal, and that these changes correlate with an individual's baseline leptin and changes in acyl-ghrelin levels respectively. Conclusions/Significance: We show that human risk preferences are exquisitely sensitive to current metabolic state, in a direction consistent with ecological models of feeding behaviour but not predicted by normative economic theory. These substantive effects of state changes on economic decisions perhaps reflect shared evolutionarily conserved neurobiological mechanisms. We suggest that this sensitivity in human risk-preference to current metabolic state has significant implications for both real-world economic transactions and for aberrant decision-making in eating disorders and obesity

Modelling Adaptation through Social Allostasis: Modulating the Effects of Social Touch with Oxytocin in Embodied Agents

Social allostasis is a mechanism of adaptation that permits individuals to dynamically adapt their physiology to changing physical and social conditions. Oxytocin (OT) is widely considered to be one of the hormones that drives and adapts social behaviours. While its precise effects remain unclear, two areas where OT may promote adaptation are by affecting social salience, and affecting internal responses of performing social behaviours. Working towards a model of dynamic adaptation through social allostasis in simulated embodied agents, and extending our previous work studying OT-inspired modulation of social salience, we present a model and experiments that investigate the effects and adaptive value of allostatic processes based on hormonal (OT) modulation of affective elements of a social behaviour. In particular, we investigate and test the effects and adaptive value of modulating the degree of satisfaction of tactile contact in a social motivation context in a small simulated agent society across different environmental challenges (related to availability of food) and effects of OT modulation of social salience as a motivational incentive. Our results show that the effects of these modulatory mechanisms have different (positive or negative) adaptive value across different groups and under different environmental circumstance in a way that supports the context-dependent nature of OT, put forward by the interactionist approach to OT modulation in biological agents. In terms of simulation models, this means that OT modulation of the mechanisms that we have described should be context-dependent in order to maximise viability of our socially adaptive agents, illustrating the relevance of social allostasis mechanisms.Peer reviewedFinal Published versio

AMPK in the central nervous system: physiological roles and pathological implications

5′ AMP-activated protein kinase (AMPK) is considered the master metabolic regulator in all eukaryotes, as it maintains cellular energy homeostasis in a variety of tissues, including the brain. In humans, alterations in AMPK activity can lead to a wide spectrum of metabolic disorders. The relevance of this protein kinase in the pathogenesis of diabetes and metabolic syndrome is now well established. On the contrary, correlations between AMPK and brain physiopathology are still poorly characterized. The aim of this review is to summarize and discuss the current knowledge about the prospective involvement of AMPK in the onset and the progression of different neurological diseases

Memory Enhancement by a Semantically Unrelated Emotional Arousal Source Induced After Learning

It has been well established that moderate physiological or emotional arousal modulates memory. However, there is some controversy about whether the source of arousal must be semantically related to the information to be remembered. To test this idea, 35 healthy young adult participants learned a list of common nouns and afterward viewed a semantically unrelated, neutral or emotionally arousing videotape. The tape was shown after learning to prevent arousal effects on encoding or attention, instead influencing memory consolidation. Heart rate increase was significantly greater in the arousal group, and negative affect was significantly less reported in the non-arousal group after the video. The arousal group remembered significantly more words than the non-arousal group at both 30 min and 24 h delays, despite comparable group memory performance prior to the arousal manipulation. These results demonstrate that emotional arousal, even from an unrelated source, is capable of modulating memory consolidation. Potential reasons for contradictory findings in some previous studies, such as the timing of “delayed” memory tests, are discussed

Beta-Adrenergic Receptor Blockade By Propranolol Enhances Retention In A Multitrial Passive-Avoidance Procedure

The effect of beta -adrenergic receptor blockade on retention in a mildly aversive passive-avoidance procedure was investigated. Rats were given passive-avoidance training-1 trial per day for 4 days-and were administered saline, the centrally and peripherally acting beta -adrenergic blocker propranolol (4 or 10 mg/kg ip), or the peripherally acting P-adrenergic blocker sotalol (4 or 10 mg/kg ip) immediately or 2 hr after the Ist trial. Enhanced retention occurred only with the higher dose (10 mg/kg) of propranolol and only when it was administered immediately after training. The enhanced retention produced by propranolol is discussed in terms of opposing, regionally specific actions of beta -adrenergic receptor-mediated neural circuits on modulation of memory