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Conférence mensuelle - Eric Stice Neural Vulnerability Factors that Increase Risk for Weight Gain

Abstract :

Conférence mensuelle Axe Cerveau et Nutrition 

Obese versus lean humans show greater reward region (caudate, amygdala, orbitofrontal cortex [OFC], insula) response to palatable food images (Bruce et al. 2010; Frankort et al., 2012; Holsen et al., 2012; Martin et al., 2009; Rothemund et al., 2007; Stice et al., 2010b; Stoeckel et al., 2008) and cues that signal impending palatable food receipt (Ng et al., 2011; Stice et al., 2008b). Critically, elevated amygdala response to palatable food images (Chouinard et al., 2010), nucleus accumbens response to palatable food images (Demos et al., 2012), OFC response to cues that predict palatable food image presentation (Yokum et al., 2011), and striatal response to palatable food commercials (Yokum et al., 2013) predict future weight gain.

Results are consistent with both the reward surfeit theory that posits that people who show greater reward region responsivity to food intake, which is presumably inborn, are at risk for overeating and weight gain (Stice et al., 2008) and the incentive sensitization theory that proposes that repeated intake of palatable foods results in an elevated reward region responsivity to cues that are associated with such food intake via conditioning, which prompts food intake when these cues are encountered (Berridge et al., 2010).

This latter theory implies that people who show more pronounced reward-cue learning should also be at risk for weight gain. A pilot study confirmed that youth who showed relatively greater increases in striatal response to cues (geometric shapes) that predicted impending milkshake receipt in a conditioning paradigm showed elevated future weight gain (Burger & Stice, submitted). Evidence suggests that thinking of the long-term health costs of eating unhealthy foods reduces reward region response to food cues, increases activation of inhibitory regions to food cues, and attenuates cravings (Kober et al., 2010; Siep et al., 2012; Yokum & Stice, 2013), implying that prevention and treatment interventions should include cognitive reappraisal training.

A pilot trial revealed that an intervention that trained young adults to apply cognitive reappraisals when confronted with unhealthy foods resulted in increased responsivity of a region implicated in inhibitory control and decreased responsivity of a region implicated in attention and expectation in response to palatable food images, but produced only pre-post reductions in weight relative to control participants that did not persist over follow-up (Stice et al., submitted). It may be possible to use real time fMRI biofeedback to increase the effects of the cognitive reappraisal obesity prevention program.

Obese versus lean adults also show less striatal D2 receptor availability (de Weijer et al., 2011; Volkow et al., 2008), lower capacity to synthesize dopamine (Wilcox et al., 2010), and weaker striatal activation in response to palatable food intake (Babbs et al., in press; Frank et al., 2012; Green et al., 2011; Stice et al., 2008a,b). Although animal experiments indicate that overfeeding reduces sensitivity of reward regions to food intake and pharmacologic stimulation (Davis et al., 2008; Geiger et al., 2009; Johnson & Kenny et al., 2010; Thanos et al., 2008), echoing effects from prospective weight gain studies with humans (Stice, Yokum, Blum, & Bohon, 2010a), it has been suggested that individuals overeat to compensate for an inborn or acquired reward deficit (Geiger et al., 2009).

However, mice in which reduced striatal DA signaling from food intake was experimentally induced through intragastric feeding of high-fat food worked less for intragastric administration of high-fat food and consumed less food ad lib than control mice (Tellez et al., 2013), which seems incompatible with the notion that an induced down-regulation of DA reward circuitry leads to compensatory overeating. In sum, whereas prospective and experimental data support the reward surfeit and incentive sensitization models of obesity, data do not support the reward deficit model.

 

Selected publications

Gearhardt, A., Yokum, S., Stice, E., Harris, J., & Brownell, K. (in press). Relation of obesity to neural activation in response to food commercials. Social Cognitive and Affective Neuroscience.

Burger, K., & Stice, E. (2014). Neural responsivity during soft drink intake, anticipation, and advertisement exposure in habitually consuming youth. Obesity, 22, 441-450.

Burger, K., & Stice, E. (2013). Elevated energy intake is correlated with hyper-responsivity in attentional, gustatory, and reward brain regions while anticipating palatable food receipt. American Journal of Clinical Nutrition, 97, 1188-1194.

Stice, E., Burger, K., & Yokum, S. (2013). Caloric deprivation increases responsivity of attention and reward regions to intake, anticipated intake, and images of palatable foods. NeuroImage, 67, 322-330.

Stice, E., Burger, K., & Yokum, S. (2013). Relative ability of fat and sugar tastes to activate reward, gustatory, and somatosensory regions. American Journal of Clinical Nutrition, 98, 1377-1384.

Stice, E., Yokum, S., & Burger, K. (2013). Elevated reward region responsivity predicts future substance use onset but not overweight/obesity onset. Biological Psychiatry, 73, 869-876.

Yokum, S., & Stice, E. (2013). Cognitive regulation of food craving: Effects of three cognitive reappraisal strategies on neural response to palatable foods. International Journal of Obesity, 37, 1565-1570.

Burger, K., & Stice, E. (2012). Frequent ice cream consumption is associated with reduced striatal response to receipt of an ice cream-based milkshake. American Journal of Clinical Nutrition, 95, 810-817.

Stice, E., Yokum, S., Burger, K., Epstein, L., & Smolen, A. (2012). Multilocus genetic composite reflecting dopamine signaling capacity predicts reward circuitry responsivity. Journal of Neuroscience, 32, 10093-10100.

Gearhardt, A., Yokum, S., Orr, P., Stice, E., Corbin, W., & Brownell, K. (2011). The neural correltes of “Food Addiction”. Archives of General Psychiatry, 68, 808-816.

Ng, J., Stice, E., Spoor, S., & Bohon, C. (2011). A brain imaging study of the relation of consummatory and anticipatory food reward to obesity: Effects of perceived caloric density. Appetite, 57, 65-72.

Stice, E., Yokum, S., Burger, K., Epstein, L., & Small, D. (2011). Youth at risk for obesity show greater activation of striatal and somatosensory regions to food. Journal of Neuroscience, 31, 4360-4366.

Yokum, S., Ng, J., & Stice, E. (2011). Attentional bias for food images associated with elevated weight and future weight gain: An fMRI study. Obesity, 19, 1775-1783.

Yokum, S., Ng, J., & Stice, E. (2011). Relation of regional grey and white matter volumes to current BMI and future increases in BMI: A prospective MRI study. International Journal of Obesity, 36, 656-664.

Batterink, L., Yokum, S., & Stice, E. (2010). Body mass correlates inversely with inhibitory control in response to food among adolescent girls: An fMRI study. NeuroImage, 1696-1703.

Stice, E., Yokum, S., Blum, K., & Bohon, C. (2010). Weight gain associated with reduced striatal response to palatable food. Journal of Neuroscience, 30, 13105-13109.

Stice, E., Yokum, S., Bohon, C., Marti, N., & Smolen, A. (2010). Reward circuitry responsivity predicts weight gain: Moderating effects of DRD2 and DRD4. NeuroImage, 50, 1618-1625.

Stice, E., Spoor, S., Bohon, C., & Small, D. (2008). Relation between obesity and blunted striatal response to food is moderated by the TaqIA1 gene. Science, 322, 4

Focus

Dr. Stice has conducted 10 prospective studies investigating risk factors for future increases in eating pathology, body mass, and depression, including 3 that have involved brain imaging, genotypes, and their interactions. He has also conducted 11 randomized efficacy and effectiveness prevention trials and 2 treatment trials targeting eating disorders, obesity, and depression. In addition, he has conducted meta-analytic reviews of risk factor studies for eating disorders and prevention trials for eating disorders, obesity, and depression. 

Agenda

Monthly Seminars

La Fédération Bordeaux Neurocampus, en concertation avec l'Ecole Doctorale SVS, met en place une série de conférences destinée à l'ensemble des étudiants effectuant leur thèse dans les laboratoires de neurosciences de la FBN.
Les doctorants seront chargés de l'organisation. Le jour de la conférence un étudiant présentera le conférencier et animera la discussion. La participation à ces conférences est fortement encouragée pour les étudiants en thèse dans les laboratoires de la fédération.


Les étudiants n'ont pas à s'inscrire pour participer à la conférence.
Ces conférences se dérouleront en anglais, salle de conférence de la Plateforme de Génomique Fonctionnelle, sont bien entendu ouvertes à tous (à toutes les disciplines même hors neurosciences).


Un lunch cloture la conférence, Il est ouvert sur inscription (une semaine à l'avance auprès de Elodie Pénicaud <elodie.penicaud@u-bordeaux.fr>, et il est limité en nombre aux premiers inscrits pour qu'il puisse y avoir une vraie discussion.
La liste des conférences, qui auront lieu tous les premiers vendredi du mois, sera publiée pour l'année. Ces conférences couvrent l'ensemble des disciplines des neurosciences bordelaises (les "axes stratégiques") et sont affichés sur le site Bordeaux Neurosciences et sur celui l'Ecole doctorale, sous la rubrique "Formation doctorale en Neurosciences". Le budget attibué à chaque conférencier sera de 1500 euros maxi.(transports, hôtel et repas)