Hedonic Hunger Is Related to Increased Neural and Perceptual Responses to Cues of Palatable Food and Motivation to Consume: Evidence from 3 Independent Investigations.

BACKGROUND: The Power of Food Scale (PFS) seeks to identify individuals who experience high appetitive drive in response to food cues, which is a construct termed "hedonic hunger." OBJECTIVE: The purpose of this study was to assess cross-sectional correlates and predictive power of PFS scores to probe the construct of hedonic hunger. METHODS: Separate data from 3 studies (study 1, n = 44; study 2, n = 398; study 3, n = 100) were used to evaluate the construct of hedonic hunger. We examined the correlations between the PFS and neural responsivity during intake and anticipated intake of palatable foods, behavioral food reinforcement, perceptual hedonic ratings of food images, and change in body mass index (BMI) and binge eating over time. RESULTS: Hedonic hunger was strongly related to bilateral brain response in regions implicated in oral somatosensory processing during cue-elicited anticipation of food intake (study 1; right postcentral gyrus: r = 0.67, P < 0.001; left postcentral gyrus: r = 0.64, P < 0.001), and was correlated with behavioral food reinforcement (study 2; r = 0.31, P = 0.03) and perceptual hedonic ratings (study 3; r = 0.24, P = 0.02). Hedonic hunger was not associated with baseline BMI (studies 1-3: P = 0.14, 0.21, and 0.37, respectively) or change in BMI over the 2-y follow-up (studies 1 and 2: P = 0.14 and 0.37, respectively) but was significantly correlated with baseline binge eating in 2 samples (study 1: r = 0.58, P = 0.001; study 2: r = 0.31, P = 0.02; and study 3: P = 0.02). CONCLUSIONS: Hedonic hunger was not predictive of weight regulation. However, individuals who report high hedonic hunger are likely to show increased neural and perceptual responses to cues of palatable foods, increased motivation to consume such foods, and a greater likelihood of current binge eating.

Elevated Thalamic Response to High-Sugar Milkshake in Ethnic and Racial Minorities.

In the USA, Hispanics and African-Americans show elevated obesity, yet little is known about possible ethnic/racial differences in brain response during intake of palatable foods. To examine potential differences between non-Hispanic white (nHW) and racial/ethnic minority individuals, we used functional magnetic resonance imaging (fMRI) to assess brain response to intake of eucaloric milkshakes that were either high-sugar or high-fat and a calorie-free, tasteless control solution. Our sample included healthy-weight adolescents who identified as African-American and/or Hispanic (minority, n = 27) and non-Hispanic white (nHW, n = 106). Minority participants showed elevated response in the pre-/postcentral gyrus, precuneus, and left thalamus in response to the high-sugar milkshake compared to high-fat milkshake. To confirm these effects were not driven by differences in body mass or a function of unequal cell sizes, we performed the same analyses in minority participants and a randomly selected subsample of nHW participants (n = 27) that were matched on BMI percentile. Similar to the full sample, we observed an elevated ventral posterior thalamic response to high-sugar milkshake in minority participants. This effect held after controlling for self-reported sugar and fat intake. These results suggest that African-American and Hispanic groups may have elevated response to specifically high-sugar foods in regions of the brain associated with sensory processing, providing novel information regarding the possible neural underpinnings of the disproportional risk for obesity seen in African-American and Hispanic populations.

Hedonic hunger prospectively predicts onset and maintenance of loss of control eating among college women.

OBJECTIVE: The subjective feeling of loss of control (LOC) over eating is common among eating-disordered individuals and has predicted weight gain in past research. Restrained eating and negative affect are risk factors for binge eating (which involves LOC), but intense feelings of pleasure derived from palatable foods might also predict the emergence or intensification of LOC eating. The Power of Food Scale (PFS) assesses preoccupation with the pleasure derived from palatable food. METHOD: The current sample (n = 294) comprised female college freshmen at risk for weight gain. LOC was assessed using an abbreviated version of the Eating Disorders Examination interview. LOC was assessed at baseline and at 6-week and 12- and 24-month follow-ups. RESULTS: Among those exhibiting LOC eating at baseline (and controlling for baseline depression, restrained eating, and body image dissatisfaction), those scoring higher on the PFS at baseline showed a smaller reduction in LOC frequency over time relative to those scoring lower. Using the same covariates, the PFS predicted the first emergence of LOC over 2 years among those showing no LOC at baseline. CONCLUSIONS: These results suggest that powerful hedonic attraction to palatable foods may represent a risk factor for the maintenance of LOC in those initially experiencing it and the emergence of LOC eating in those who are not. An enhanced ability to identify individuals at increased risk of developing or maintaining LOC eating could be useful in prevention programs.

Leptin signaling in the medial nucleus tractus solitarius reduces food seeking and willingness to work for food.

The adipose-derived hormone leptin signals in the medial nucleus tractus solitarius (mNTS) to suppress food intake, in part, by amplifying within-meal gastrointestinal (GI) satiation signals. Here we show that mNTS leptin receptor (LepRb) signaling also reduces appetitive and motivational aspects of feeding, and that these effects can depend on energy status. Using the lowest dose that significantly suppressed 3-h cumulative food intake, unilateral leptin (0.3 µg) administration to the mNTS (3 h before testing) reduced operant lever pressing for sucrose under increasing work demands (progressive ratio reinforcement schedule) regardless of whether animals were energy deplete (food restricted) or replete (ad libitum fed). However, in a separate test of food-motivated responding in which there was no opportunity to consume food (conditioned place preference (CPP) for an environment previously associated with a palatable food reward), mNTS leptin administration suppressed food-seeking behavior only in chronically food-restricted rats. On the other hand, mNTS LepRb signaling did not reduce CPP expression for morphine reinforcement regardless of energy status, suggesting that mNTS leptin signaling differentially influences motivated responding for food vs opioid reward. Overall results show that mNTS LepRb signaling reduces food intake and appetitive food-motivated responding independent of energy status in situations involving orosensory and postingestive contact with food, whereas food-seeking behavior independent of food consumption is only reduced by mNTS LepRb activation in a state of energy deficit. These findings reveal a novel appetitive role for LepRb signaling in the mNTS, a brain region traditionally linked with processing of meal-related GI satiation signals.

Hippocampal leptin signaling reduces food intake and modulates food-related memory processing.

The increase in obesity prevalence highlights the need for a more comprehensive understanding of the neural systems controlling food intake; one that extends beyond food intake driven by metabolic need and considers that driven by higher-order cognitive factors. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. Here we examine whether administration of the adiposity hormone leptin to the dorsal and ventral sub-regions of the hippocampus influences food intake and memory for food. Leptin (0.1 µg) delivered bilaterally to the ventral hippocampus suppressed food intake and body weight measured 24 h after administration; a higher dose (0.4 µg) was needed to suppress intake following dorsal hippocampal delivery. Leptin administration to the ventral but not dorsal hippocampus blocked the expression of a conditioned place preference for food and increased the latency to run for food in an operant runway paradigm. Additionally, ventral but not dorsal hippocampal leptin delivery suppressed memory consolidation for the spatial location of food, whereas hippocampal leptin delivery had no effect on memory consolidation in a non-spatial appetitive response paradigm. Collectively these findings indicate that ventral hippocampal leptin signaling contributes to the inhibition of food-related memories elicited by contextual stimuli. To conclude, the results support a role for hippocampal leptin signaling in the control of food intake and food-related memory processing.