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Food Decision-Making: Effects of Weight Status and Age

Floor van Meer, Lisette Charbonnier, and Paul A. M. Smeets

Current Diabetes Reports (2016) 16: 84

Food decisions determine energy intake. Since overconsumption is the main driver of obesity, the effects of weight status on food decision-making are of increasing interest. An additional factor of interest is age, given the rise in childhood obesity, weight gain with aging, and the increased chance of type 2 diabetes in the elderly. The effects of weight status and age on food preference, food cue sensitivity, and self-control are discussed, as these are important components of food decision-making. Furthermore, the neural correlates of food anticipation and choice and how these are affected by weight status and age are discussed. Behavioral studies show that in particular, poor self-control may have an adverse effect on food choice in children and adults with overweight and obesity. Neuroimaging studies show that overweight and obese individuals have altered neural responses to food in brain areas related to reward, self-control, and interoception. Longitudinal studies across the lifespan will be invaluable to unravel the causal factors driving (changes in) food choice, overconsumption, and weight gain.

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Do Europeans like Nudges?

Lucia A. Reisch and Cass R Sunstein

Judgement and Decision Making Vol 11 No 4 July 2016 310-325

In recent years, many governments have shown a keen interest in “nudges” — approaches to law and policy that maintain freedom of choice, but that steer people in certain directions. Yet to date, there has been little evidence on whether citizens of various societies support nudges and nudging. We report the results of nationally representative surveys in six European nations: Denmark, France, Germany, Hungary, Italy, and the United Kingdom. We find strong majority support for nudges of the sort that have been adopted, or under serious consideration, in democratic nations. Despite the general European consensus, we find markedly lower levels of support for nudges in two nations: Hungary and Denmark. We are not, in general, able to connect support for nudges with distinct party affiliations.

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Brain Insulin Resistance at the Crossroads of Metabolic and Cognitive Disorders in Humans

Stephanie Kullmann, Martin Heni, Manfred Hallschmid, Andreas Fritsche, Hubert Preissl, and Hans-Ulrich Häring

Physiological Reviews 96: 1169-1209 2016

Ever since the brain was identified as an insulin-sensitive organ, evidence has rapidly accumulated that insulin action in the brain produces multiple behavioral and metabolic effects, influencing eating behavior, peripheral metabolism, and cognition. Disturbances in brain insulin action can be observed in obesity and type 2 diabetes (T2D), as well as in aging and dementia. Decreases in insulin sensitivity of central nervous pathways, i.e., brain insulin resistance, may therefore constitute a joint pathological feature of metabolic and cognitive dysfunctions. Modern neuroimaging methods have provided new means of probing brain insulin action, revealing the influence of insulin on both global and regional brain function. In this review, we highlight recent findings on brain insulin action in humans and its impact on metabolism and cognition. Furthermore, we elaborate on the most prominent factors associated with brain insulin resistance, i.e., obesity, T2D, genes, maternal metabolism, normal aging, inflammation, and dementia, and on their roles regarding causes and consequences of brain insulin resistance. We also describe the beneficial effects of enhanced brain insulin signaling on human eating behavior and cognition and discuss potential applications in the treatment of metabolic and cognitive disorders.

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Modulation of attentional networks by food-related disinhibition

Maike A. Hege, Krunoslav T. Stingl, Ralf Veit, and Hubert Preissl

Physiology & Behaviour 176 (2017) 84-92

The risk of weight gain is especially related to disinhibition, which indicates the responsiveness to external food stimuli with associated disruptions in eating control. We adapted a food-related version of the attention network task and used functional magnetic resonance imaging to study the effects of disinhibition on attentional networks in 19 normal-weight participants. High disinhibition scores were associated with a rapid reorienting response to food pictures after invalid cueing and with an enhanced alerting effect of awarning cue signalizing the upcoming appearance of a food picture. Imaging data revealed activation of a right-lateralized ventral attention network during reorienting. The faster the reorienting and the higher the disinhibition score, the less activation of this network was observed. The alerting contrast showed activation in visual, temporo-parietal and anterior sites. These modulations of attentional networks by food-related disinhibition might be related to an attentional bias to energy dense and palatable food and increased intake of food in disinhibited individuals.

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Food Decision-Making: Effects of Weight Status and Age

Floor van Meer, Lisette Charbonnier  & Paul A. M. Smeets

Current Diabetes Reports (2016) 16:84

Food decisions determine energy intake. Since overconsumption is the main driver of obesity, the effects of weight status on food decision-making are of increasing interest. An additional factor of interest is age, given the rise in
childhood obesity, weight gain with aging, and the increased chance of type 2 diabetes in the elderly. The effects of weight status and age on food preference, food cue sensitivity, and self-control are discussed, as these are important components of food decision-making. Furthermore, the neural correlates of food anticipation and choice and how these are affected by weight status and age are discussed. Behavioral studies show that in particular, poor self-control may have an adverse effect on food choice in children and adults with overweight and obesity. Neuroimaging studies show that overweight and obese individuals have altered neural responses to food in brain areas related to reward, self-control, and interoception. Longitudinal studies across the lifespan will be invaluable to unravel the causal factors driving (changes in) food choice over-consumption, and weight gain.

read the full article

GLP-1 and estrogen conjugate acts in the supramammillary nucleus to reduce food-reward and body weight

Heike Vogel, Stefanie Wolf, Cristina Rabasa, Francisca Rodriguez-Pacheco, Carina S. Babaei, Franziska Stober, Jürgen Goldschmidt, Richard D. DiMarchi, Brian Finan , Matthias H. Tschop , Suzanne L. Dickson , Annette Schürmann, Karolina P. Skibicka

Neuropharmacology 110 (2016) 396-406

The obesity epidemic continues unabated and currently available pharmacological treatments are not sufficiently effective. Combining gut/brain peptide, GLP-1, with estrogen into a conjugate may represent a novel, safe and potent, strategy to treat diabesity. Here we demonstrate that the central administration of GLP-1-estrogen conjugate reduced food reward, food intake, and body weight in rats. In order to determine the brain location of the interaction of GLP-1 with estrogen, we avail of single-photon emission computed tomography imaging of regional cerebral blood flow and pinpoint a brain site unexplored for its role in feeding and reward, the supramammillary nucleus (SUM) as a potential target of the conjugated GLP-1-estrogen. We confirm that conjugated GLP-1 and estrogen directly target the SUM
with site-specific microinjections. Additional microinjections of GLP-1-estrogen into classic energy balance controlling nuclei, the lateral hypothalamus (LH) and the nucleus of the solitary tract (NTS) revealed that the metabolic benefits resulting from GLP-1-estrogen injections are mediated through the LH and to some extent by the NTS. In contrast, no additional benefit of the conjugate was noted on food reward when the compound was microinjected into the LH or the NTS, identifying the SUM as the only neural substrate identified here to underlie the reward reducing benefits of GLP-1 and estrogen conjugate. Collectively we discover a surprising neural substrate underlying food intake and reward effects of GLP-1 and estrogen and uncover a new brain area capable of regulating energy balance and reward.

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Genetic predisposition to obesity affects behavioural traits includingfood reward and anxiety-like behaviour in rats

Heike Vogel, Maria Kraemer, Cristina Rabasa, Kaisa Askevik, Roger A.H. Adan,Suzanne L. Dickson

Behavioural Brain Research, 328 (2017) 95-104

tHere we sought to define behavioural traits linked to anxiety, reward, and exploration in different strainsof rats commonly used in obesity research. We hypothesized that genetic variance may contributenot only to their metabolic phenotype (that is well documented) but also to the expression of thesebehavioural traits. Rat strains that differ in their susceptibility to develop an obese phenotype (Sprague-Dawley, Obese Prone, Obese Resistant, and Zucker rats) were exposed to a number of behavioural testsstarting at the age of 8 weeks. We found a similar phenotype in the obesity susceptible models, ObeseProne and Zucker rats, with a lower locomotor activity, exploratory activity, and higher level of anxiety-like behaviour in comparison to the leaner Obese Resistant strain. We did not find evidence that rat strainswith a genetic predisposition to obesity differed in their ability to experience reward from chocolate (ina condition place preference task). However, Zucker rats show higher motivated behaviour for sucrosecompared to Obese Resistant rats when the effort required to obtain palatable food is relatively low.Together our data demonstrate that rat strains that differ in their genetic predisposition to developobesity also differ in their performance in behavioural tests linked to anxiety, exploration, and rewardand that these differences are independent of body weight. We conclude that genetic variations whichdetermine body weight and the aforementioned behaviours co-exist but that future studies are requiredto identify whether (and which) common genes are involved.

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The determinants of food choice

Gareth Leng, Roger A. H. Adan, Michele Belot, Jeffrey M. Brunstrom, Kees de Graaf, Suzanne L. Dickson, Todd Hare, Silvia Maier, John Menzies, Hubert Preissl, Lucia A. Reisch, Peter J. Rogers and Paul A. M. Smeets

in "Proceedings of the Nutrition Society" ,  Summer Meeting University College Dublin July 2016

Conference on ‘New technology in nutrition research and practice’

Health nudge interventions to steer people into healthier lifestyles are increasingly applied by governments worldwide, and it is natural to look to such approaches to improve health by altering what people choose to eat. However, to produce policy recommendations that are likely to be effective, we need to be able to make valid predictions about the consequences of proposed interventions, and for this, we need a better understanding of the determinants of food choice. These determinants include dietary components (e.g. highly palatable foods and alcohol), but also diverse cultural and social pressures, cognitive-affective factors (perceived stress, health attitude, anxiety and depression), and familial, genetic and epigenetic influences on personality characteristics. In addition, our choices are influenced by an array of physiological mechanisms, including signals to the brain from the gastrointestinal tract and adipose tissue, which affect not only our hunger and satiety but also our motivation to eat particular nutrients, and the reward we experience from eating. Thus, to develop the evidence base necessary for effective policies, we need to build bridges across different levels of knowledge and understanding. This requires experimental models that can fill in the gaps in our understanding that are needed to inform policy, translational models that connect mechanistic understanding from laboratory studies to the real life human condition, and formal models that encapsulate scientific knowledge from diverse disciplines, and which embed understanding in a way that enables policy-relevant predictions to be made. Here we review recent developments in these areas.

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Spike patterning in oxytocin neurons: Capturing physiological behaviour with Hodgkin-Huxley and integrate-and-fire models

Gareth Leng, Trystan Leng, Duncan J MacGregor

PlosONE, 12 (7) 2107

Integrate-and-fire (IF) models can provide close matches to the discharge activity of neurons, but do they oversimplify the biophysical properties of the neurons? A single compartment Hodgkin-Huxley (HH) model of the oxytocin neuron has previously been developed, incorporating biophysical measurements of channel properties obtained in vitro. A simpler modified integrate-and-fire model has also been developed, which can match well the characteristic spike patterning of oxytocin neurons as observed in vivo. Here, we extended the HH model to incorporate synaptic input, to enable us to compare spike activity in the model with experimental data obtained in vivo. We refined the HH model parameters to closely match the data, and then matched the same experimental data with a modified IF model, using an evolutionary algorithm to optimise parameter matching. Finally we compared the properties of the modified HH model with those of the IF model to seek an explanation for differences between spike patterning in vitro and in vivo. We show that, with slight modifications, the original HH model, like the IF model, is able to closely match both the interspike interval (ISI) distributions of oxytocin neurons and the observed variability of spike firing rates in vivo and in vitro. This close match of both models to data depends on the presence of a slow activity-dependent hyperpolarisation (AHP); this is represented in both models and the parameters used in the HH model representation match well with optimal parameters of the IF model found by an evolutionary algorithm. The ability of both models to fit data closely also depends on a shorter hyperpolarising after potential (HAP); this is explicitly represented in the IF model, but in the HH model, it emerges from a combination of several components. The critical elements of this combination are identified.

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Individual variability in preference for energy-dense foods fails to predict child BMI percentile

Christina Potter, Rebecca L. Griggs, Danielle Ferriday, Peter J. Rogers, Jeffrey M. Brunstrom

Physiology & Behaviour 176 (2017) 3-8

Many studies show that higher dietary energy density is associated with greater body weight. Here we explored two propositions: i) that child BMI percentile is associated with individual differences in children's relative preference for energy-dense foods, ii) that child BMI percentile is associated with the same individual differences between their parents. Child-parent dyads were recruited from a local interactive science center in Bristol (UK). Using computerized tasks, participants ranked their preference and rated their liking for a range of snack foods that varied in energy density. Children (aged 3–14 years, N=110) and parents completed the tasks for themselves. Parents also completed two further tasks in which they ranked the foods in the order that they would prioritize for their child, and again, in the order that they thought their child would choose. Children preferred (t(109) =3.91, p < 0.001) and better liked the taste of (t(109) =3.28, p=0.001) higher energy-dense foods, and parents correctly estimated this outcome (t(109) = 7.18, p < 0.001). Conversely, lower energy-dense foods were preferred (t(109) =−4.63, p < 0.001), better liked (t(109) =−2.75, p=0.007) and served (t(109) = −15.06, p < 0.001) by parents. However, we found no evidence that child BMI percentile was associated with child or parent preference for, or liking of, energy-dense foods. Therefore, we suggest that the observed
relationship between dietary energy density and body weight is not explained by individual differences in preference for energy density.

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