Understanding weight-related differences in functional connectivity provides key insight into neurocognitive factors implicated in obesity. Here, we sampled three groups from human connectome project data: 1) 47 pairs of BMI-discordant twins (n=94; average BMI-discordancy 6.7 3.1 kg/m2), 2) 47 pairs of gender and BMI matched BMI-discordant, unrelated individuals, and 3) 47 pairs of BMI-similar twins to test for body mass dependent differences in between network functional connectivity. Across BMI discordant samples, three networks appeared to be highly sensitivity to weight status; specifically, a network compromised of gustatory processing regions, a visual processing network, and the default mode network (DMN). Further, individuals with a lower BMI relative to their twin had stronger connectivity between striatal/thalamic and prefrontal networks (pFWE = 0.04) in the BMI-discordant twin sample. Cortical-striatal-thalamic networks underlie regulation of hedonically motivated behaviors. Stronger connectivity may facilitate increased regulation of decision-making when presented with highly rewarding, energy-dense foods. We also observed that individuals with a higher BMI than their twin had stronger connectivity between cerebellar and insular networks (pFWE = 0.04). Increased cerebellar-insula connectivity is associated with caloric deprivation and, in high BMI individuals, is associated compromised satiation signaling, thereby increasing risk for postprandial food intake. Connectivity patterns observed in the BMI-discordant twin sample were not see in a BMI-similar sample, providing evidence that the results are specific to BMI discordance. Beyond the involvement of gustatory and visual networks and the DMN, little overlap in results were seen between the two BMI-discordant samples. This may be a function of the higher study design sensitivity in the BMI-discordant twin sample, relative to the more generalizable results in the unrelated sample. These […]
Advances in neuroimaging techniques have provided insight into the role of the brain in the regulation of food intake and weight. Growing evidence demonstrate that energy dense, palatable foods elicit similar responses in reward-related brain regions that mimic those of addictive substances. Currently, various models of obesity’s relation to reward from food have been theorized. There is evidence to support a theory of hypo-responsivity of reward regions to food, where individuals consume excess amounts to overcome this reward deficit. There is also data to support a theory of hyper-responsivity of reward regions, where individuals who experience greater reward from food intake are at risk for overeating. However, these seemingly discordant theories are static in nature and do not account for the possible effects of repeated overeating on brain responsivity to food and initial vulnerability factors. Here we review data that support these theories and propose a dynamic vulnerability model of obesity that appears to offer a parsimonious theory that accommodates extant findings.
Theorists posit that food reward is a powerful determinant of intake, yet little is known regarding how individuals’ hedonic ratings of a variety of foods inter-relate and how hedonic ratings correspond to habitual dietary intake. Participant ratings of food appeal of 104 food images were collected while participants were in a fed state (n=129). Self-reported frequency of intake of the food items, perceived hunger, body mass index (BMI), and dietary restraint were also assessed. Principal components analysis (PCA) was employed to analyze hedonic ratings of the foods, to identify component structures and to reduce the number of variables. The resulting component structures comprised 63 images loading on 7 components including Energy-Dense Main Courses, Light Main Courses and Seafood as well as components more analogous to traditional food groups (e.g., Fruits, Grains, Desserts, Meats). However, vegetables were not represented in a unique, independent component. All components were positively correlated with reported intake of the food items (r’s = 0.26 - 0.52,
As no large prospective study has evaluated neural vulnerability factors that predict future weight gain we tested whether neural response to receipt and anticipated receipt of palatable food and monetary reward predicted weight gain over 3-year follow-up in originally healthy-weight adolescents and whether relations were moderated by the TaqIA polymorphism, which affects dopamine signaling capacity. 153 adolescent humans completed functional magnetic resonance imaging (fMRI) paradigms assessing response to these four events; body fat was assessed yearly over follow-up. Split half analyses indicated that elevated orbitofrontal cortex response to cues signaling impending milkshake receipt predicted future body fat gain (r = .32), which is a novel finding that provides support for the incentive sensitization theory of obesity. Neural response to receipt and anticipated receipt of monetary reward did not predict body fat gain, which has not been tested previously. Replicating an interaction reported previously (Stice et al., 2008a), elevated caudate response to milkshake receipt predicted future body fat gain for youth with a genetic propensity for greater dopamine signaling by virtue of possessing the TaqIA A2/A2 allele, but lower caudate response predicted body fat gain for youth with a genetic propensity for less dopamine signaling by virtue of possessing a TaqIA A1 allele, though this interaction was only marginal (pFWE = .06). Parental obesity, which correlated with TaqIA allele status (OR = 2.7), similarly moderated the predictive effects of caudate response to milkshake receipt to body fat gain, which is also a novel finding. The former interaction implies that too much or too little dopamine signaling capacity and reward region responsivity may increase risk for overeating, suggesting the possibility of qualitatively distinct reward surfeit and reward deficit pathways to obesity.
Prospective studies indicate that individuals with elevated dietary restraint scores are at increased risk for future bulimic symptom onset, suggesting that these individuals may show hyper-responsivity of reward regions to food and food cues. Thus, we used functional magnetic resonance imaging (fMRI) to examine the relation of dietary restraint scores to activation of reward-related brain regions in response to receipt and anticipated receipt of chocolate milkshake and exposure to pictures of appetizing foods in 39 female adolescents (mean age = 15.5 ± 0.94). Dietary restraint scores were positively correlated with activation in the right orbitofrontal cortex (OFC) and bilateral dorsolateral prefrontal cortex (DLPFC) in response to milkshake receipt. However, dietary restraint scores did not correlate with activation in response to anticipated milkshake receipt or exposure to food pictures. Results indicate that individuals who report high dietary restraint have a hyper-responsivity in reward-related brain regions when food intake is occurring, which may increase risk for overeating and binge eating.
OBJECTIVE: Although soft drinks are heavily advertised, widely consumed, and have been associated with obesity, little is understood regarding neural responsivity to soft drink intake, anticipated intake, and advertisements. METHODS: Functional MRI was used to assess examine neural response to carbonated soft drink intake, anticipated intake and advertisement exposure as well as milkshake intake in 27 adolescents that varied on soft drink consumer status. RESULTS: Intake and anticipated intake of carbonated Coke® activated regions implicated in gustatory, oral somatosensory, and reward processing, yet high-fat/sugar milkshake intake elicited greater activation in these regions versus Coke intake. Advertisements highlighting the Coke product vs. non-food control advertisements, but not the Coke logo, activated gustatory and visual brain regions. Habitual Coke consumers vs. non-consumers showed greater posterior cingulate responsivity to Coke logo ads, suggesting that the logo is a conditioned cue. Coke consumers exhibited less ventrolateral prefrontal cortex responsivity during anticipated Coke intake relative to non-consumers. CONCLUSIONS: Results indicate that soft drinks activate reward and gustatory regions, but are less potent in activating these regions than high-fat/sugar beverages, and imply that habitual soft drink intake promotes hyper-responsivity of regions encoding salience/attention toward brand specific cues and hypo-responsivity of inhibitory regions while anticipating intake.
Animal experiments indicate that after repeated pairings of palatable food receipt and cues that predict palatable food receipt, dopamine signaling increases in response to predictive cues, but decreases in response to food receipt. Using functional MRI and mixed effects growth curve models with 35 females (M age=15.5±0.9; M BMI=24.5±5.4) we documented an increase in BOLD response in the caudate (r=.42) during exposure to cues predicting impending milkshake receipt over repeated exposures, demonstrating a direct measure of in vivo cue-reward learning in humans. Further, we observed a simultaneous decrease in putamen (r=-.33) and ventral pallidum (r=-.45) response during milkshake receipt that occurred over repeated exposures, putatively reflecting food reward habitation. We then tested whether cue-reward learning and habituation slopes predicted future weight over 2-year follow-up. Those who exhibited the greatest escalation in ventral pallidum responsivity to cues and the greatest decrease in caudate response to milkshake receipt showed significantly larger increases in BMI (r=.39 and -.69 respectively). Interestingly, cue-reward learning propensity and food reward habituation were not correlated, implying that these factors may constitute qualitatively distinct vulnerability pathways to excess weight gain. These two individual difference factors may provide insight as to why certain people have shown obesity onset in response to the current obesogenic environment in western cultures, whereas others have not.
Caloric intake and energy balance are highly regulated to maintain metabolic homeostasis and weight. However, hedonic motivated food intake, in particular consumption of highly rewarding foods, may act to override hemostatic signaling and contribute to overconsumption, weight gain and obesity. Here, we review human neuroimaging literature that has delivered valuable insight into the neural correlates of hedonic motivated ingestive behavior, weight gain, weight loss and metabolic status. Our primary focus is the brain regions that are thought to encode aspects of food hedonics, gustatory and somatosensory processing, and executive functioning. Further, we discuss the variability of regional brain response as a function of obesity, weight gain, behavioral and surgical weight loss, as well as in type 2 diabetes.
Background: Visual presentation of food provides considerable information such as its potential for palatability and availability, both of which can impact eating behavior. Methods: We investigated the subjective ratings for food appeal and desire to eat when exposed to food pictures in a fed sample (n=129) using the computer paradigm ImageRate. Food appeal and desire to eat were analyzed for the effects of food group, portion size and energy density of the foods presented as well as by participant characteristics. Results: Food appeal ratings were significantly higher than those for desire to eat (57.9 ± 11.6 v. 44.7 ± 18.0;
Adequate energy intake is vital for the survival of humans and is regulated by complex homeostatic and hedonic mechanisms. Supported by functional MRI (fMRI) studies that consistently demonstrate differences in brain response as a function of weight status during exposure to appetizing food stimuli, it has been posited that hedonically driven food intake contributes to weight gain and obesity maintenance. These food reward theories of obesity are reliant on the notion that the aberrant brain response to food stimuli relates directly to ingestive behavior, specifically, excess food intake. However current studies frequently use weight as a dependent measure, and homeostatic neuroendocrine regulators of food intake, such as leptin and ghrelin, are also impacted by weight status. Importantly, these differences endocrine functioning may contribute to effects seen in fMRI studies of reward-related obesity. In the present review, we examine the relative influence of weight and weight change, exogenous administration of appetitive hormones, and measures of ingestive behavior on BOLD response to food stimuli. Emerging evidence implicating the influences of impulsivity, macronutrient content, and reward learning and habituation in ingestive behavior and obesity are also considered.
Increases in portion size lead to increases in energy intake, yet the mechanisms behind this ‘portion size effect’ are unclear. This study tested possible mechanisms of the portion size effect i.e., bite size and visual cues in 30 over- and normal-weight individuals (15 men, 15 women). A 2x2 repeated measures, within-subject design was used to test the effects of portion size (410g vs. 820g of a pasta dish) and visual cues (blindfolded vs. visible) on energy intake. At each meal participants were exposed to one of four experimental conditions (small portion/visible; small portion/blindfold; large portion/visible; large portion/blindfold). Participant characteristics, food intake, number of bites, meal duration, palatability measures and hunger and fullness were assessed. In response to a doubling of the portion presented, entrée energy intake increased 26% (220kcal P
Children of overweight/obese parents are at a high-risk of developing obesity. This study sought to examine the underlying neural factors related to parental obesity risk and the relative impact of sugar and fat when consuming a palatable food, as well as the impact of obesity risk status on brain response to appetizing food images. Using functional MRI, 108 healthy weight adolescents’ (BMI 20.9±1.9; n=53 high-risk by virtue of parental obesity status, n=55 low-risk) response to food stimuli were examined. Stimuli included four milkshakes systematically varied in sugar and fat content, a calorie-free tasteless solution, and images of appetizing foods and glasses of water. High risk vs. low risk adolescents showed greater BOLD response to milkshakes (all variants collapsed) > tasteless solution receipt in the primary gustatory and oral somatosensory cortices (pFWE tasteless solution contrast, however an effect of risk status was not seen in the high-fat milkshake contrast (pFWE