Evidence that a novel transdiagnostic eating disorder treatment reduces reward region response to the thin beauty ideal and high-calorie binge foods.

BACKGROUND: Findings from brain imaging studies with small samples can show limited reproducibility. Thus, we tested whether the evidence that a transdiagnostic eating disorder treatment reduces responsivity of brain valuation regions to thin models and high-calorie binge foods, the intervention targets, from a smaller earlier trial emerged when we recruited additional participants. METHODS: Women with DSM-5 eating disorders (N = 138) were randomized to the dissonance-based body project treatment (BPT) or a waitlist control condition and completed functional magnetic resonance imaging (fMRI) scans assessing neural response to thin models and high-calorie foods at pretest and posttest. RESULTS: BPT v. control participants showed significantly greater reductions in responsivity of regions implicated in reward valuation (caudate) and attentional motivation (precuneus) to thin v. average-weight models, echoing findings from the smaller sample. Data from this larger sample also provided novel evidence that BPT v. control participants showed greater reductions in responsivity of regions implicated in reward valuation (ventrolateral prefrontal cortex) and food craving (hippocampus) to high-calorie binge foods v. low-calorie foods, as well as significantly greater reductions in eating disorder symptoms, abstinence from binge eating and purging behaviors, palatability ratings for high calorie foods, monetary value for high-calorie binge foods, and significantly greater increases in attractiveness ratings of average weight models. CONCLUSIONS: Results from this larger sample provide evidence that BPT reduces valuation of the thin ideal and high-calorie binge foods, the intervention targets, per objective brain imaging data, and produces clinically meaningful reductions in eating pathology.

The association of adolescents' television viewing with Body Mass Index percentile, food addiction, and addictive phone use.

Television (TV) viewing remain a popular forms of screen time for adolescents. Greater TV viewing is associated with a number of negative consequences for adolescent health. In a changing media landscape, it is important to understand adolescents' overall and commercial TV exposure, and how TV viewing is linked to health risks (e.g., obesity, food addiction, and phone addiction). The purpose of this study was to: 1) examine differences by age, gender, race/ethnicity, and parental education in overall TV and commercial TV viewing and 2) investigate whether adolescents who watch more overall TV and commercial TV programming were more likely to have a higher BMI percentile, more addictive eating, and more addictive phone use. A sample of 190 adolescents (13-16 years of age) completed Time-Use Diaries (TUDs) in 2015-2017. We found that girls had more overall weekday TV time than males. No other gender differences were detected for weekend TV time or commercial TV time. Higher BMI percentile was not correlated with greater overall or commercial TV viewing. However, we did identify a positive association between overall TV viewing and commercial TV viewing with addictive-eating and addictive phone use. This effect was mainly driven by boys. To our knowledge, this is the first study to investigate patterns of television viewing and addictive-like eating and addictive phone use. We conclude that adolescents, particularly boys, with higher TV viewing may be more likely to present with problems with addictive eating behavior and phone use. Our findings add to the research on the behavioral health correlates of TV viewing among adolescents.

Gain in Body Fat Is Associated with Increased Striatal Response to Palatable Food Cues, whereas Body Fat Stability Is Associated with Decreased Striatal Response.

UNLABELLED: Cross-sectional brain-imaging studies reveal that obese versus lean humans show greater responsivity of reward and attention regions to palatable food cues, but lower responsivity of reward regions to palatable food receipt. However, these individual differences in responsivity may result from a period of overeating. We conducted a repeated-measures fMRI study to test whether healthy weight adolescent humans who gained body fat over a 2 or 3 year follow-up period show an increase in responsivity of reward and attention regions to a cue signaling impending milkshake receipt and a simultaneous decrease in responsivity of reward regions to milkshake receipt versus adolescents who showed stability of or loss of body fat. Adolescents who gained body fat, who largely remained in a healthy weight range, showed increases in activation in the putamen, mid-insula, Rolandic operculum, and precuneus to a cue signaling impending milkshake receipt versus those who showed stability of or loss of body fat, though these effects were partially driven by reductions in responsivity among the latter groups. Adolescents who gained body fat reported significantly greater milkshake wanting and milkshake pleasantness ratings at follow-up compared to those who lost body fat. Adolescents who gained body fat did not show a reduction in responsivity of reward regions to milkshake receipt or changes in responsivity to receipt and anticipated receipt of monetary reward. Data suggest that initiating a prolonged period of overeating may increase striatal responsivity to food cues, and that maintaining a balance between caloric intake and expenditure may reduce striatal, insular, and Rolandic operculum responsivity. SIGNIFICANCE STATEMENT: This novel, repeated-measures brain-imaging study suggests that adolescents who gained body fat over our follow-up period experienced an increase in striatal responsivity to cues for palatable foods compared to those who showed stability of or loss of body fat. Results also imply that maintaining a balance between caloric intake and expenditure over time may reduce striatal, insular, and Rolandic operculum responsivity to food cues, which might decrease risk for future overeating.

Reward Region Responsivity Predicts Future Weight Gain and Moderating Effects of the TaqIA Allele.

Because no large prospective study has investigated 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 body fat gain over a 3-year follow-up in healthy-weight adolescent humans and whether the TaqIA polymorphism moderates these relations. A total of 153 adolescents completed fMRI paradigms assessing response to these events; body fat was assessed annually over follow-up. Elevated orbitofrontal cortex response to cues signaling impending milkshake receipt predicted future body fat gain (r = 0.32), 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 earlier finding (Stice et al., 2008a), elevated caudate response to milkshake receipt predicted body fat gain for adolescents 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 adolescents with a genetic propensity for less dopamine signaling by virtue of possessing a TaqIA A1 allele, though this interaction was only marginal [p-value <0.05 corrected using voxel-level familywise error rate (pFWE) = 0.06]. Parental obesity, which correlated with TaqIA allele status (odds ratio = 2.7), similarly moderated the relation of caudate response to milkshake receipt to future body fat gain, which is another novel finding. The former interaction implies that too much or too little dopamine signaling and reward region responsivity increases risk for overeating, suggesting qualitatively distinct reward surfeit and reward deficit pathways to obesity. SIGNIFICANCE STATEMENT: Because no large prospective study has investigated 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 body fat gain over 3-year follow-up in healthy-weight adolescent humans and whether the TaqIA polymorphism moderates these relations. Elevated reward activation in response to food cues predicted future body fat gain. Elevated reward response to food receipt predicted body fat gain for adolescents with a TaqIA A2/A2 allele and lower reward response predicted body fat gain for those with a TaqIA A1 allele. Results imply that too much or too little dopamine signaling and reward region responsivity increases risk for overeating.

Relation of the multilocus genetic composite reflecting high dopamine signaling capacity to future increases in BMI.

Because food intake exerts its rewarding effect by increasing dopamine (DA) signaling in reward circuitry, it theoretically follows that individuals with a greater number of genotypes putatively associated with high DA signaling capacity are at increased risk for overeating and subsequent weight gain. We tested the association between the multilocus genetic composite risk score, defined by the total number of genotypes putatively associated with greater DA signaling capacity (i.e. TaqIA A2 allele, DRD2-141C Ins/Del and Del/Del genotypes, DRD4-S allele, DAT1-S allele, and COMT Val/Val genotype), and future increases in Body Mass Index (BMI) in three prospective studies. Participants in Study 1 (N = 30; M age = 15.2; M baseline BMI = 26.9), Study 2 (N = 34; M age = 20.9; M baseline BMI = 28.2), and Study 3 (N = 162; M age = 15.3, M baseline BMI = 20.8) provided saliva samples from which epithelial cells were collected, permitting DNA extraction. The multilocus genetic composite risk score was associated with future increases in BMI in all three studies (Study 1, r = 0.37; Study 2, r = 0.22; Study 3, r = 0.14) and the overall sample (r = 0.19). DRD4-S was associated with increases in BMI in Study 1 (r = 0.42), Study 2 (r = 0.27), and in the overall sample (r = 0.17). DAT1-S was associated with increases in BMI in Study 3 (r = 0.17) and in the overall sample (r = 0.12). There were no associations between the other genotypes (TaqIA, COMT, and DRD2-141C) and change in BMI over 2-year follow-up. Data suggest that individuals with a genetic propensity for greater DA signaling capacity are at risk for future weight gain and that combining alleles that theoretically have a similar function may provide a more reliable method of modeling genetic risk associated with future weight gain than individual genotypes.

Food reinforcement and parental obesity predict future weight gain in non-obese adolescents.

BACKGROUND: Food reinforcement, the extent to which people are willing to work to earn a preferred snack food, and parental obesity are risk factors for weight gain, but there is no research comparing the predictive effects of these factors for adolescent weight gain. METHODS: 130 non-obese adolescents (M age=15.2 ± 1.0; M BMI=20.7 ± 2.0; M zBMI=0.16 ± 0.64) at differential risk for weight gain based on parental obesity completed baseline food and money reinforcement tasks, and provided zBMI data over a 2-year follow-up. RESULTS: The number of obese (BMI ≥ 30) parents (p=0.007) and high food reinforcement (p=0.046) were both significant independent predictors of greater zBMI increases, controlling for age, sex, parent education and minority status. Having no obese parents or being low or average in food reinforcement was associated with reductions in zBMI, but those high in food reinforcement showed larger zBMI increases (0.102) than having one obese parent (0.025) but less than having two obese parents (0.177). DISCUSSION: Food reinforcement and parental obesity independently predict future weight gain among adolescents. It might be fruitful for obesity prevention programs to target both high risk groups.

Multilocus genetic composite reflecting dopamine signaling capacity predicts reward circuitry responsivity.

The objective of the study was to test the hypotheses that humans with genotypes putatively associated with low dopamine (DA) signaling capacity, including the TaqIA A1 allele, DRD2-141C Ins/Ins genotype, DRD4 7-repeat or longer allele, DAT1 10-repeat allele, and the Met/Met COMT genotype, and with a greater number of these genotypes per a multilocus composite, show less responsivity of reward regions that primarily rely on DA signaling. Functional magnetic resonance imaging (fMRI) paradigms were used to investigate activation in response to receipt and anticipated receipt of palatable food and monetary reward. DNA was extracted from saliva using standard methods. Participants were 160 adolescents (mean age = 15.3 years, SD = 1.07 years; mean body mass index = 20.8, SD = 1.9). The main outcome was blood oxygenation level-dependent activation in the fMRI paradigms. Data confirmed that these fMRI paradigms activated reward, attention, somatosensory, and gustatory regions. Individuals with, versus without, these five genotypes did not show less activation of DA-based reward regions, but those with the Met/Met versus the Val/Val COMT genotype showed less middle temporal gyrus activation and those with the DRD4-L versus the DRD4-S genotype showed less middle occipital gyrus activation in response to monetary reward. Critically, the multilocus composite score revealed that those with a greater number of these genotypes showed less activation in reward regions, including the putamen, caudate, and insula, in response to monetary reward. The results suggest that the multilocus genetic composite is a more sensitive index of vulnerability for low reward region responsivity than individual genotypes.

Caloric deprivation increases responsivity of attention and reward brain regions to intake, anticipated intake, and images of palatable foods.

Dietary restraint theoretically increases risk for binge eating, but prospective and experimental studies have produced contradictory findings, apparently because dietary restraint scales do not identify individuals who are reducing caloric intake. Yet, experimentally manipulated caloric deprivation increases responsivity of brain regions implicated in attention and reward to food images, which may contribute to binge eating. We tested whether self-imposed acute and longer-term caloric restriction increases responsivity of attention and reward regions to images, anticipated receipt, and receipt of palatable food using functional magnetic resonance imaging among female and male adolescents (Study 1 n=34; Study 2 n=51/81). Duration of acute caloric deprivation correlated positively with activation in regions implicated in attention, reward, and motivation in response to images, anticipated receipt, and receipt of palatable food (e.g., anterior cingulate cortex, orbitofrontal cortex, putamen, and precentral gyrus respectively). Youth in a longer-term negative energy balance likewise showed greater activation in attention (anterior cingulate cortex, ventral medial prefrontal cortex), visual processing (superior visual cortex), reward (caudate) and memory (hippocampus) regions in response to receipt and anticipated receipt of palatable food relative to those in neutral or positive energy balance. Results confirm that self-imposed caloric deprivation increases responsivity of attention, reward, and motivation regions to food, which may explain why caloric deprivation weight loss diets typically do not produce lasting weight loss.

Eating disorder prevention: current evidence-base and future directions.

OBJECTIVE: This narrative review sought to (a) characterize prevention programs that have produced reliable, reproducible, and clinically meaningful effects in efficacy trials, (b) discuss effectiveness trials that have tested whether prevention programs produce intervention effects under ecologically valid real-world conditions, (c) discuss dissemination efforts and research on dissemination, and (d) offer suggestions regarding directions for future research in this field. CONCLUSION: A literature revealed that 6 prevention programs have produced significant reductions in eating disorder symptoms through at least 6-month follow-up and that 2 have significantly reduced future eating disorder onset. Effectiveness trials indicate that 2 prevention programs have produced effects under ecologically valid conditions that are only slightly attenuated. Although there have been few dissemination efforts, evidence suggests that a community participatory approach is most effective. Lastly, it would be useful to develop programs that produce larger and more persistent reductions in eating disorder symptoms and eating disorder onset, focus more on effectiveness trials that confirm that prevention programs produce clinically meaningful effects under real-world conditions, conduct meditational, mechanisms of action, and moderator research that provides stronger support for the intervention theory of prevention programs, and investigate the optimal methods of disseminating and implementing evidence-based prevention programs.

Elevated reward, emotion, and memory region response to thin models predicts eating disorder symptom persistence: A prospective functional magnetic resonance imaging study.

Because few studies have identified biological factors that predict the persistence of eating pathology, we tested the hypotheses that elevated responsivity of brain regions implicated in reward valuation to thin models and high-calorie binge foods would predict the persistence of eating pathology. We analyzed data from 146 women (Mage = 21.87 ± 3.81) with threshold or subthreshold anorexia nervosa, bulimia nervosa, binge eating disorder, or purging disorder who completed functional magnetic resonance imaging scans assessing neural response to thin models and binge foods at baseline, were randomized to two eating disorder treatments or a waitlist control condition and completed diagnostic interviews that assessed change in symptoms over 2.5-month follow-up. Elevated activation in regions associated with memory (parahippocampal gyrus r = .38; hippocampus r = .25) and with reward valuation and emotional salience (amygdala r = .35) in response to thin versus average-weight models predicted future persistence of an eating disorder symptom composite (all analyses controlled for treatment condition). Neural response to high-calorie binge foods did not predict the persistence of eating disorder symptoms. There was no evidence that either treatment moderated the relation of baseline neural responsivity to thin models to future persistence of eating disorder symptoms, though power for these post hoc analyses was limited. Results suggest that overvaluation of the thin ideal increases the risk for the persistence of eating disorder symptoms but provided no support for the hypothesis that overvaluation of high-calorie foods would predict symptom persistence. Results imply that treatments should seek to reduce the overvaluation of the thin ideal. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Relation of BOLD response to food-specific and generic motor response inhibition tasks to body fat gain in adults with overweight and obesity.

BACKGROUND: Low inhibitory control has been theorized to contribute to the development and maintenance of obesity. Knowledge on the neurobiological indicators of inhibitory control deficits predicting future weight gain is limited. The current study examined if individual differences in blood-oxygenation-level-dependent (BOLD) activity associated with food-specific and general motor response inhibition predict future body fat change in adults with overweight or obesity. METHODS: BOLD activity and behavioral responses of adults with overweight or obesity (N = 160) were recorded while performing a food-specific stop signal task (n = 92) or a generic stop signal task (n = 68). Percent body fat was measured at baseline, posttest, 3-month, and 6-month follow-up. RESULTS: Elevated BOLD activity in somatosensory (postcentral gyrus), and attention (precuneus) regions during successful inhibition in the food-specific stop signal task and elevated BOLD activity in a motor region (anterior cerebellar lobe) in the generic stop signal task predicted greater body fat gain over 6-month follow-up. Elevated BOLD activity in inhibitory control regions (inferior-, middle-, superior frontal gyri) and error monitoring regions (anterior cingulate cortex, insula) during erroneous responses in the generic stop signal task predicted body fat loss. CONCLUSIONS: Results suggest that improving motor response inhibition and error monitoring may facilitate weight loss in adults with overweight and obesity.

Relation of Overweight/Obesity to Reward Region Response to Food Reward and the Moderating Effects of Parental History of Eating Pathology in Adolescent Females.

OBJECTIVE: To test whether overweight/obesity is associated with an elevated reward region response to milkshake cues and a low reward region response to milkshake receipt. To test whether the risk for eating pathology moderates the effects of weight status on the neural response to milkshake cues and milkshake receipt. METHOD: The current study used functional magnetic resonance imaging (fMRI) to examine the neuronal responses of female adolescents (n = 80; M age = 14.6 ± 0.9; M BMI = 21.9 ± 3.6; 41% with a biological parental history of eating pathology) during a food receipt paradigm. RESULTS: Females with overweight/obesity showed a greater ventromedial prefrontal cortex (vmPFC), and ventral anterior cingulate (ACC) response to milkshake cues and a greater ventral striatum, subgenual ACC, and dorsomedial prefrontal cortex response to milkshake receipt than those with a healthy weight. Females with overweight/obesity plus a parental history of eating pathology showed a greater vmPFC/medial orbitofrontal cortex response to milkshake cues than those without a parental history of eating pathology and those with a healthy weight. Females with overweight/obesity and without a parental history of eating pathology showed a greater thalamus and striatum response to milkshake receipt. CONCLUSIONS: Overweight/obesity is associated with an elevated reward region response to palatable food cues and food receipt. A risk for eating pathology enhances the reward region response to food cues in those with excess weight.

A randomized trial of two group-delivered transdiagnostic eating disorder treatments: Dissonance-based treatment versus interpersonal psychotherapy.

OBJECTIVE: Test whether a group-delivered dissonance-based transdiagnostic eating disorder treatment, Body Project Treatment (BPT), produces greater reductions in eating disorder symptoms and higher abstinence from eating disorder behaviors and remittance from eating disorder diagnoses than group-delivered transdiagnostic interpersonal psychotherapy (IPT). METHOD: Women with a range of eating disorders (N = 73) were randomized to 8-week group-implemented BPT or IPT and completed surveys and masked diagnostic interviews at pretest, posttest, and 6-month follow-up. RESULTS: Participants randomized to BPT versus IPT showed significantly greater reductions in eating disorder symptoms (d = -.75), pursuit of the thin ideal (d = -.87), anxiety symptoms (d = -.76), and social impairment (d = -.59) through 6-month follow-up. By end of treatment, participants randomized to the BPT versus IPT did not significantly differ on abstinence from binge eating and purging (49% vs. 40%, respectively) or remittance from eating disorder diagnoses (54% vs. 40%, respectively). Participants randomized to BPT versus IPT did not differ significantly in average session attendance (5.8 vs. 6.9, respectively) or average homework assignments completed (4.6 vs. 5.6, respectively). The within-condition reductions in eating disorder symptoms for BPT did not significantly differ when implemented in person versus via synchronous video telepsychiatry (d = -1.39 vs. -1.09, respectively), though these effects should be considered preliminary because of the small cell sizes. CONCLUSIONS: The evidence that BPT produces greater reductions in eating disorder symptoms, pursuit of the thin ideal, anxiety symptoms, and social impairment than IPT is encouraging because it provides some assurance that the effects are present equating for the effects of expectancies, demand characteristics, and nonspecific factors. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Correlates of neural adaptation to food cues and taste: the role of obesity risk factors.

Identifying correlates of brain response to food cues and taste provides critical information on individual differences that may influence variability in eating behavior. However, a few studies examine how brain response changes over repeated exposures and the individual factors that are associated with these changes. Using functional magnetic resonance imaging, we examined how brain response to a palatable taste and proceeding cues changed over repeated exposures and how individual differences in weight, familial obesity risk, dietary restraint and reward responsiveness correlate with these changes. In healthy-weight adolescents (n = 154), caudate and posterior cingulate cortex (PCC) response increased with repeated cue presentations, and oral somatosensory cortex and insula response increased with repeated milkshake tastes. The magnitude of increase over exposures in the left PCC to cues was positively associated with body mass index percentile (r = 0.18, P = 0.026) and negatively associated with dietary restraint scores (r = -0.24, P = 0.003). Adolescents with familial obesity risk showed higher cue-evoked caudate response across time, compared to the low-risk group (r = 0.12, P = 0.035). Reward responsiveness positively correlated with right oral somatosensory cortex/insula response to milkshake over time (r = 0.19, P = 0.018). The results show that neural responses to food cues and taste change over time and that individual differences related to weight gain are correlated with these changes.

Youth at risk for obesity show greater activation of striatal and somatosensory regions to food.

Obese humans, compared with normal-weight humans, have less striatal D2 receptors and striatal response to food intake; 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 humans also show greater striatal, amygdalar, orbitofrontal cortex, and somatosensory region response to food images than normal-weight humans do, 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. Using fMRI, 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. 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.

Efficacy of a combined food-response inhibition and attention training for weight loss.

This Current Opinion in Behavioral Sciences article reviews trials that evaluated an obesity treatment that combines response-inhibition training with high-calorie foods and training designed to reduce attention for high-calorie foods. Two randomized controlled trials suggest that food-response inhibition and attention training produced significant body-fat loss, along with a reduction in valuation of, and reward-region response to, high-calorie foods. However, these effects did not emerge in a third trial, potentially because this trial used more heterogeneous food images, which reduced inhibition learning and attentional learning. Collectively, results suggest that food-response inhibition and attention training can devalue high-calorie foods and result in weight loss, but only if a homogeneous set of high-calorie and low-calorie food images is used.

Efficacy of a food response and attention training treatment for obesity: A randomized placebo controlled trial.

Elevated brain reward and attention region response, and weaker inhibitory region response to high-calorie foods has predicted future weight gain, suggesting that an intervention that reduces reward and attention region response and increases inhibitory region response to such foods might reduce overeating. We conducted a randomized controlled trial to test whether a multi-faceted food response and attention training protocol with personalized high- and low-calorie food images would reduce body fat and valuation and reward region response to high-calorie foods compared to a placebo control training protocol with non-food images in an effort to replicate findings from two past trials. Participants were community-recruited adults with overweight/obesity (N = 179; M age = 27.7 ± 7.0) who completed assessments at pretest, posttest, 3-month, 6-month, and 12-month follow-ups. Participants randomized to the food response inhibition and attention training showed significantly greater increases in palatability ratings of low-calorie foods than controls (d = 0.27) at posttest, but did not show body fat loss, reductions in palatability ratings and monetary valuation, or reward region response, to high-calorie foods. The lack of expected effects appears to be related to weaker learning compared to the learning in past trials, potentially because we used more heterogenous high-calorie and low-calorie food images in the present training.

Weight gain is associated with reduced striatal response to palatable food.

Consistent with the theory that individuals with hypofunctioning reward circuitry overeat to compensate for a reward deficit, obese versus lean humans have fewer striatal D2 receptors and show less striatal response to palatable food intake. Low striatal response to food intake predicts future weight gain in those at genetic risk for reduced signaling of dopamine-based reward circuitry. Yet animal studies indicate that intake of palatable food results in downregulation of D2 receptors, reduced D2 sensitivity, and decreased reward sensitivity, implying that overeating may contribute to reduced striatal responsivity. Thus, we tested whether overeating leads to reduced striatal responsivity to palatable food intake in humans using repeated-measures functional magnetic resonance imaging. Results indicated that women who gained weight over a 6 month period showed a reduction in striatal response to palatable food consumption relative to weight-stable women. Collectively, results suggest that low sensitivity of reward circuitry increases risk for overeating and that this overeating may further attenuate responsivity of reward circuitry in a feedforward process.

An fMRI study of obesity, food reward, and perceived caloric density. Does a low-fat label make food less appealing?

We tested the hypothesis that obese individuals experience greater activation of the gustatory and somatosensory cortex, but weaker activation of the striatum, in response to intake and anticipated intake of high-fat chocolate milkshake versus an isocaloric milkshake labeled low-fat and a tasteless solution using functional magnetic resonance imaging (fMRI) with 17 obese and 17 lean young women. Obese relative to lean women showed greater activation in somatosensory (Rolandic operculum), gustatory (frontal operculum), and reward valuation regions (amgydala, ventralmedial prefrontal cortex (vmPFC) in response to intake and anticipated intake of milkshake versus tasteless solution, though there was little evidence of reduced striatal activation. Obese relative to lean women also showed greater activation in the Rolandic operculum, frontal operculum, and vmPFC in response to isocaloric milkshakes labeled regular versus low-fat. Results suggest that hyper-responsivity of somatosensory, gustatory, and reward valuation regions may be related to overeating and that top-down processing influence reward encoding, which could further contribute to weight gain.

Neural Vulnerability Factors That Predict Future Weight Gain.

PURPOSE OF REVIEW: The current article discusses five neural vulnerability theories for weight gain and reviews evidence from prospective studies using imaging and behavioral measures reflecting neural function, as well as randomized experiments with humans and animals that are consistent or inconsistent with these theories. RECENT FINDINGS: Recent prospective imaging studies examining predictors of weight gain and response to obesity treatment, and repeated-measures imaging studies before and after weight gain and loss have advanced knowledge of etiologic processes and neural plasticity resulting from weight change. Overall, data provide strong support for the incentive sensitization theory of obesity and moderate support for the reward surfeit theory, inhibitory control deficit theory, and dynamic vulnerability model of obesity, which attempted to synthesize the former theories into a single etiologic model. Data provide little support for the reward deficit theory. Important directions for future studies are delineated.