We performed successive H(2)(15)O-PET scans on volunteers as they ate chocolate to beyond satiety. Thus, the sensory stimulus and act (eating) were held constant while the reward value of the chocolate and motivation of the subject to eat were manipulated by feeding. Non-specific effects of satiety (such as feelings of fullness and autonomic changes) were also present and probably contributed to the modulation of brain activity. After eating each piece of chocolate, subjects gave ratings of how pleasant/unpleasant the chocolate was and of how much they did or did not want another piece of chocolate. Regional cerebral blood flow was then regressed against subjects' ratings. Different groups of structures were recruited selectively depending on whether subjects were eating chocolate when they were highly motivated to eat and rated the chocolate as very pleasant [subcallosal region, caudomedial orbitofrontal cortex (OFC), insula/operculum, striatum and midbrain] or whether they ate chocolate despite being satiated (parahippocampal gyrus, caudolateral OFC and prefrontal regions). As predicted, modulation was observed in cortical chemosensory areas, including the insula and caudomedial and caudolateral OFC, suggesting that the reward value of food is represented here. Of particular interest, the medial and lateral caudal OFC showed opposite patterns of activity. This pattern of activity indicates that there may be a functional segregation of the neural representation of reward and punishment within this region. The only brain region that was active during both positive and negative compared with neutral conditions was the posterior cingulate cortex. Therefore, these results support the hypothesis that there are two separate motivational systems: one orchestrating approach and another avoidance behaviours.

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese relative to lean individuals, suggesting that the striatum and dopaminergic signaling in the striatum may contribute to development of obesity. Thus, we tested whether striatal activation in response to food intake is related to current and future increases in body mass and whether these relations are moderated by presence of the A1 allele of the TaqlA1 gene, which is associated with compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, suggesting that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.Although twin studies suggest that biological factors play a major role in the etiology of obesity, few prospective studies have identified biological factors that increase risk for future weight gain. Dopamine is involved in the reinforcing effects of food (1). Feeding is associated with dopamine release in the dorsal striatum and the degree of pleasure from eating correlates with amount of dopamine release (2,3). The dorsal striatum responds to ingestion of chocolate in lean humans and is sensitive to its devaluation by feeding beyond satiety (4). In contrast, the ventral striatum appears to respond to food receipt only if it is unexpected (5) and plays a preferential role in encoding the value of cues associated with food receipt, responding preferentially to cues versus receipt (6) and showing sensitivity to the devaluation of food cues, but not food receipt (4,7). Thus, the dorsal and ventral striatum may serve distinct roles in encoding food reward, with the former playing a more prominent role in encoding consummatory food reward. Dopamine antagonists increase appetite, energy intake, and weight gain, whereas dopamine agonists reduce energy intake and produce weight loss (8,9). Dopamine D2 receptors are reduced in obese relative to lean individuals (10,11). Obese rats have lower basal dopamine levels and reduced D2 receptor expression than lean rats (12,13). It has thus been postulated that obese individuals have hypofunctioning reward circuitry, which leads them to overeat to compensate for a hypofunctioning dopamine reward system (14).We used blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) to test whether obese relative to lean individuals show abnormal activation of the dorsal

We tested the hypothesis that obese individuals experience greater reward from food consumption (consummatory food reward) and anticipated consumption (anticipatory food reward) than lean individuals using functional magnetic resonance imaging (fMRI) with 33 adolescent girls (M age = 15.7 SD = 0.9). Obese relative to lean adolescent girls showed greater activation bilaterally in the gustatory cortex (anterior and mid insula, frontal operculum) and in somatosensory regions (parietal operculum and Rolandic operculum) in response to anticipated intake of chocolate milkshake (versus a tasteless solution) and to actual consumption of milkshake (versus a tasteless solution); these brain regions encode the sensory and hedonic aspects of food. However, obese relative to lean adolescent girls also showed decreased activation in the caudate nucleus in response to consumption of milkshake versus a tasteless solution, potentially because they have reduced dopamine receptor availability. Results suggest that individuals who show greater activation in the gustatory cortex and somatosensory regions in response to anticipation and consumption of food, but who show weaker activation in the striatum during food intake, may be at risk for overeating and consequent weight gain. Keywordsobesity; anticipatory food reward; consummatory food reward; fMRI Obesity is a chronic disease that is credited with over 111,000 deaths annually in the US, which largely result from atherosclerotic cerebrovascular disease, coronary heart disease, colorectal cancer, hyperlipidemia, hypertension, gallbladder disease, and diabetes mellitus (Flegal, Graubard, Williamson, & Gail, 2005). Regrettably, the treatment of choice for obesity only results in transitory weight loss (Jeffery et al., 2000) and most obesity prevention programs do not reduce risk for future weight gain (Stice, Shaw, & Marti, 2006). These interventions may have limited efficacy because our understanding of the etiologic processes is still incomplete. Although it has been established that obesity is the result of a positive energy balance, it is Correspondence should be addressed to Eric Stice, who is at Oregon Research Institute, 1715 Franklin Blvd., Eugene, Oregon, 97403. Email: E-mail: estice@ori.org. 3 Based on the evidence that reward-related neural function in women is heightened during the mid-follicular phase (Dreher et al., 2007), we created a dichotomous variable that reflected whether participants completed the fMRI scans during the midfollicular phase (days 4-8 after onset of menses; n = 2) or not (n = 31). When we controlled for this variable in all analyses, the activation in the reported regions remained significant. One possible explanation is that some individuals have abnormalities in subjective reward from food intake or anticipated intake that increase risk for obesity. Some scholars hypothesize that obese individuals experience greater activation of the meso-limbic reward system in response to food intake (consummatory food reward), which may increase risk ...

We used a 2 x 2 factorial design to dissociate regions responding to taste intensity and taste affective valence. Two intensities each of a pleasant and unpleasant taste were presented to subjects during event-related fMRI scanning. The cerebellum, pons, middle insula, and amygdala responded to intensity irrespective of valence. In contrast, valence-specific responses were observed in anterior insula/operculum extending into the orbitofrontal cortex (OFC). The right caudolateral OFC responded preferentially to pleasant compared to unpleasant taste, irrespective of intensity, and the left dorsal anterior insula/operculuar region responded preferentially to unpleasant compared to pleasant tastes equated for intensity. Responses best characterized as an interaction between intensity and pleasantness were also observed in several limbic regions. These findings demonstrate a functional segregation within the human gustatory system. They also show that amygdala activity may be driven by stimulus intensity irrespective of valence, casting doubt upon the notion that the amygdala responds preferentially to negative stimuli.

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Perceptions of the flavors of foods or beverages reflect information derived from multiple sensory afferents, including gustatory, olfactory, and somatosensory fibers. Although flavor perception therefore arises from the central integration of multiple sensory inputs, it is possible to distinguish the different modalities contributing to flavor, especially when attention is drawn to particular sensory characteristics. Nevertheless, our experiences of the flavor of a food or beverage are also simultaneously of an overall unitary perception. Research aimed at understanding the mechanisms behind this integrated flavor perception is, for the most part, relatively recent. However, psychophysical, neuroimaging and neurophysiological studies on cross-modal sensory interactions involved in flavor perception have started to provide an understanding of the integrated activity of sensory systems that generate such unitary perceptions, and hence the mechanisms by which these signals are "functionally united when anatomically separated". Here we review this recent research on odor/taste integration, and propose a model of flavor processing that depends on prior experience with the particular combination of sensory inputs, temporal and spatial concurrence, and attentional allocation. We propose that flavor perception depends upon neural processes occurring in chemosensory regions of the brain, including the anterior insula, frontal operculum, orbitofrontal cortex and anterior cingulate cortex, as well as upon the interaction of this chemosensory "flavor network" with other heteromodal regions including the posterior parietal cortex and possibly the ventral lateral prefrontal cortex.

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Obese versus normal-weight humans have less striatal D2 receptors and striatal response to food intake, and weaker striatal response to food predicts weight gain for individuals at genetic risk for reduced dopamine (DA) signaling, consistent with the reward deficit theory of obesity. Yet these may not be initial vulnerability factors, as overeating reduces D2 receptor density, D2 sensitivity, reward sensitivity, and striatal response to food. Obese versus normal-weight humans also show greater striatal, amygdalar, orbitofrontal cortex, and somatosensory region response to food images, which predicts weight gain for those not at genetic risk for compromised dopamine signaling, consonant with the reward surfeit theory of obesity. However, after pairings of palatable food intake and predictive cues, DA signaling increases in response to the cues, implying that eating palatable food contributes to increased responsivity. We tested whether normal-weight adolescents at high- versus low-risk for obesity showed aberrant activation of reward circuitry in response to receipt and anticipated receipt of palatable food and monetary reward using fMRI. High-risk youth showed greater activation in the caudate, parietal operculum, and frontal operculum in response to food intake and in the caudate, putamen, insula, thalamus, and orbitofrontal cortex in response to monetary reward. No differences emerged in response to anticipated food or monetary reward. Data indicate that youth at risk for obesity show elevated reward circuitry responsivity in general coupled with elevated somatosensory region responsivity to food, which may lead to overeating that produces blunted dopamine signaling and elevated responsivity to food cues.