Sonja Yokum

Oregon Research Institute, Eugene, Oregon, United States

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Publications (20)103.24 Total impact

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    ABSTRACT: Objective Adolescents view thousands of food commercials annually, but little is known about how individual differences in neural response to food commercials relate to weight gain. To add to our understanding of individual risk factors for unhealthy weight gain and environmental contributions to the obesity epidemic, we tested the associations between reward region (striatum and orbitofrontal cortex [OFC]) responsivity to food commercials and future change in body mass index (BMI).Methods Adolescents (N = 30) underwent a scan session at baseline while watching a television show edited to include 20 food commercials and 20 nonfood commercials. BMI was measured at baseline and 1-year follow-up.ResultsActivation in the striatum, but not OFC, in response to food commercials relative to nonfood commercials and in response to food commercials relative to the television show was positively associated with change in BMI over 1-year follow-up. Baseline BMI did not moderate these effects.Conclusions The results suggest that there are individual differences in neural susceptibility to food advertising. These findings highlight a potential mechanism for the impact of food marketing on adolescent obesity.
    Obesity 08/2014; · 3.92 Impact Factor
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    ABSTRACT: 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.
    Appetite 07/2014; · 2.54 Impact Factor
  • Eric Stice, Kyle S Burger, Sonja Yokum
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    ABSTRACT: Although the intake of high-fat and high-sugar food activates mesolimbic reward, gustatory, and oral somatosensory brain regions, contributing to overeating, few studies have examined the relative role of fat and sugar in the activation of these brain regions, which would inform policy, prevention, and treatment interventions designed to reduce obesity. We evaluated the effect of a high-fat or high-sugar equicaloric chocolate milkshake and increasing fat or sugar milkshake content on the activation of these regions. Functional magnetic resonance imaging was used to assess the neural response to the intake of high-fat/high-sugar, high-fat/low-sugar, low-fat/high-sugar, and low-fat/low-sugar chocolate milkshakes and a tasteless solution in 106 lean adolescents (mean ± SD age = 15.00 ± 0.88 y). Analyses contrasted the activation to the various milkshakes. High-fat compared with high-sugar equicaloric milkshakes caused greater activation in the bilateral caudate, postcentral gyrus, hippocampus, and inferior frontal gyrus. High-sugar compared with high-fat equicaloric milkshakes caused greater activation in the bilateral insula extending into the putamen, the Rolandic operculum, and thalamus, which produced large activation regions. Increasing sugar in low-fat milkshakes caused greater activation in the bilateral insula and Rolandic operculum; increasing fat content did not elicit greater activation in any region. Fat caused greater activation of the caudate and oral somatosensory regions than did sugar, sugar caused greater activation in the putamen and gustatory regions than did fat, increasing sugar caused greater activity in gustatory regions, and increasing fat did not affect the activation. Results imply that sugar more effectively recruits reward and gustatory regions, suggesting that policy, prevention, and treatment interventions should prioritize reductions in sugar intake. This trial was registered at clinicaltrials.gov as DK092468.
    American Journal of Clinical Nutrition 10/2013; · 6.50 Impact Factor
  • Eric Stice, Sonja Yokum
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    ABSTRACT: The present study tested the competing hypotheses that adolescents at risk for future substance abuse and dependence by virtue of parental substance use disorders show either weaker or stronger responsivity of brain regions implicated in reward relative to youth without parental history of substance use disorders. Adolescents (n = 52) matched on demographics with and without parental substance use disorders, as determined by diagnostic interviews, who denied substance use in the past year were compared on functional MRI (fMRI) paradigms assessing neural response to receipt and anticipated receipt of monetary and food reward. Parental-history-positive versus -negative adolescents showed greater activation in the left dorsolateral prefrontal cortex and bilateral putamen, and less activation in the fusiform gyrus and inferior temporal gyrus in response to anticipating winning money, as well as greater activation in the left midbrain and right paracentral lobule, and less activation in the right middle frontal gyrus in response to milkshake receipt. Results indicate that adolescents at risk for future onset of substance use disorders show elevated responsivity of brain regions implicated in reward, extending results from 2 smaller prior studies that found that individuals with versus without parental alcohol use disorders showed greater reward region response to anticipated monetary reward and pictures of alcohol. Collectively, results provide support for the reward surfeit model of substance use disorders, rather than the reward deficit model. (PsycINFO Database Record (c) 2013 APA, all rights reserved).
    Psychology of Addictive Behaviors 10/2013; · 2.09 Impact Factor
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    ABSTRACT: 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. © 2013 by Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:478-485).
    International Journal of Eating Disorders 07/2013; 46(5):478-85. · 3.03 Impact Factor
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    ABSTRACT: Adolescents view thousands of food commercials annually, but the neural response to food advertising and its association with obesity is largely unknown. The current study is the first to examine how neural response to food commercials differs from other stimuli (e.g., non-food commercials, television show) and to explore how this response may differ by weight status. The blood oxygen level-dependent functional magnetic resonance imaging activation was measured in thirty adolescents ranging from lean to obese in response to food and non-food commercials imbedded in a television show. Adolescents exhibited greater activation in regions implicated in visual processing (e.g., occipital gyrus), attention (e.g., parietal lobes), cognition (e.g., temporal gyrus, posterior cerebellar lobe), movement (e.g., anterior cerebellar cortex), somatosensory response (e.g., postcentral gyrus), and reward (e.g., orbitofrontal cortex, anterior cingulate cortex (ACC)) during food commercials. Obese participants exhibited less activation during food relative to non-food commercials in neural regions implicated in visual processing (e.g., cuneus), attention (e.g., posterior cerebellar lobe), reward (e.g., ventromedial prefrontal cortex, ACC) and salience detection (e.g., precuneus). Obese participants did exhibit greater activation in a region implicated in semantic control (e.g., medial temporal gyrus). These findings may inform current policy debates regarding the impact of food advertising to minors.
    Social Cognitive and Affective Neuroscience 04/2013; · 5.04 Impact Factor
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    S Yokum, E Stice
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    ABSTRACT: Objective:Obese versus lean individuals show greater reward region and reduced inhibitory region responsivity to food images, which predict future weight gain. Thinking of the costs of eating palatable foods and craving suppression have been found to modulate this neural responsivity, but these cognitive reappraisal studies have primarily involved lean participants. Herein we evaluated the efficacy of a broader range of reappraisal strategies in modulating neural responsivity to palatable food images among individuals who ranged from lean to obese and tested whether body mass index (BMI) moderates the effects of these strategies.Materials and methods:Functional magnetic resonance imaging assessed the effects of three cognitive reappraisal strategies in response to palatable food images versus an imagined intake comparison condition in a sample of adolescents (N=21; M age=15.2).Results:Thinking of the long-term costs of eating the food, thinking of the long-term benefits of not eating the food and attempting to suppress cravings for the food increased activation in inhibitory regions (for example, superior frontal gyrus, ventrolateral prefrontal cortex) and reduced activation in attention-related regions (for example, precuneus and posterior cingulate cortex). The reappraisal strategy focusing on the long-term benefits of not eating the food more effectively increased inhibitory region activity and reduced attention region activity compared with the other two cognitive reappraisal strategies. BMI did not moderate the effects.Discussion:These novel results imply that cognitive reappraisal strategies, in particular those focusing on the benefits of not eating the food, could potentially increase the ability to inhibit appetitive motivation and reduce unhealthy food intake in overweight individuals.International Journal of Obesity advance online publication, 9 April 2013; doi:10.1038/ijo.2013.39.
    International journal of obesity (2005) 04/2013; · 5.22 Impact Factor
  • Eric Stice, Sonja Yokum, Kyle S Burger
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    ABSTRACT: BACKGROUND: We tested the hypotheses that adolescents who show elevated reward region responsivity are at increased risk for initial onset of overweight/obesity and substance use, which is important because there have been no such prospective tests of the reward surfeit model of these motivated behaviors. METHODS: One hundred sixty-two adolescents (mean age = 15.3±1.06 years) with healthy weights (mean body mass index = 20.8±1.90) completed functional magnetic resonance imaging paradigms that assessed neural activation in response to receipt and anticipated receipt of palatable food and monetary reward; body fat and substance use were assessed at baseline and 1-year follow-up. RESULTS: Elevated caudate (r = .31, p<.001) and putamen (r = .28, p<.001) response to monetary reward predicted substance use onset over 1-year follow-up, but reward circuitry responsivity did not predict future overweight/obesity onset. Adolescents who reported substance use versus abstinence at baseline also showed less caudate (r =-.31, p<.001) response to monetary reward. DISCUSSION: Results show that hyper-responsivity of reward circuitry increases risk for future substance use onset, providing novel support for the reward surfeit model. Results also imply that even a limited substance use history was associated with reduced reward region responsivity, extending results from studies that compared substance-dependent individuals with healthy control subjects and suggesting that substance use downregulates reward circuitry. However, aberrant reward region responsivity did not predict initial unhealthy weight gain.
    Biological psychiatry 01/2013; · 8.93 Impact Factor
  • Eric Stice, Kyle Burger, Sonja Yokum
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    ABSTRACT: 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 1N=34; Study 2N=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.
    NeuroImage 11/2012; · 6.25 Impact Factor
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    ABSTRACT: 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.
    Journal of Neuroscience 07/2012; 32(29):10093-100. · 6.91 Impact Factor
  • S Yokum, J Ng, E Stice
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    ABSTRACT: This study tested whether global and regional brain volumes correlated with body mass index (BMI) and increases in BMI over 1-year follow-up. A total of 83 young females (M age=18.4, s.d.=2.8; BMI range=17.3-38.9) were scanned using magnetic resonance imaging. Voxel-based morphometry was used to assess global brain volume and regional gray matter (GM) and white matter (WM) volumes in regions implicated in taste, reward and inhibitory control. Obese participants had less total GM volume than lean and overweight participants. Obese participants had lower total WM volume than overweight participants. BMI correlated with higher WM volumes in the middle temporal gyrus, fusiform gyrus, parahippocampal gyrus, Rolandic operculum and dorsal striatum. Trend-level reduced GM volumes in the superior frontal gyrus and middle frontal gyrus were related to increases in BMI over 1-year follow-up. Findings suggest that BMI is related to global and regional differences in brain matter volume in female adolescents. Most importantly, findings suggest that low GM volume in regions implicated in inhibitory control are related to future weight gain. Results taken in conjunction with prior findings suggest that abnormalities in regional GM volumes, but not WM volumes, increase the risk for future weight gain and abnormalities in regional WM volumes, but not GM volumes, are secondary to weight gain.
    International journal of obesity (2005) 09/2011; 36(5):656-64. · 5.22 Impact Factor
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    Sonja Yokum, Janet Ng, Eric Stice
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    ABSTRACT: Behavioral studies reveal that obese vs. lean individuals show attentional bias to food stimuli. Yet research has not investigated this relation using objective brain imaging or tested whether attentional bias to food stimuli predicts future weight gain, which are important aims given the prominence of food cues in the environment. We used functional magnetic resonance imaging (fMRI) to examine attentional bias in 35 adolescent girls ranging from lean to obese using an attention network task involving food and neutral stimuli. BMI correlated positively with speed of behavioral response to both appetizing food stimuli and unappetizing food stimuli, but not to neutral stimuli. BMI correlated positively with activation in brain regions related to attention and food reward, including the anterior insula/frontal operculum, lateral orbitofrontal cortex (OFC), ventrolateral prefrontal cortex (vlPFC), and superior parietal lobe, during initial orientation to food cues. BMI also correlated with greater activation in the anterior insula/frontal operculum during reallocation of attention to appetizing food images and with weaker activation in the medial OFC and ventral pallidum during reallocation of attention to unappetizing food images. Greater lateral OFC activation during initial orientation to appetizing food cues predicted future increases in BMI. Results indicate that overweight is related to greater attentional bias to food cues and that youth who show elevated reward circuitry responsivity during food cue exposure are at increased risk for weight gain.
    Obesity 06/2011; 19(9):1775-83. · 3.92 Impact Factor
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    Janet Ng, Eric Stice, Sonja Yokum, Cara Bohon
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    ABSTRACT: 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.
    Appetite 04/2011; 57(1):65-72. · 2.54 Impact Factor
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    ABSTRACT: Research has implicated an addictive process in the development and maintenance of obesity. Although parallels in neural functioning between obesity and substance dependence have been found, to our knowledge, no studies have examined the neural correlates of addictive-like eating behavior. To test the hypothesis that elevated "food addiction" scores are associated with similar patterns of neural activation as substance dependence. Between-subjects functional magnetic resonance imaging study. A university neuroimaging center. Forty-eight healthy young women ranging from lean to obese recruited for a healthy weight maintenance trial. The relation between elevated food addiction scores and blood oxygen level-dependent functional magnetic resonance imaging activation in response to receipt and anticipated receipt of palatable food (chocolate milkshake). Food addiction scores (N = 39) correlated with greater activation in the anterior cingulate cortex, medial orbitofrontal cortex, and amygdala in response to anticipated receipt of food (P < .05, false discovery rate corrected for multiple comparisons in small volumes). Participants with higher (n = 15) vs lower (n = 11) food addiction scores showed greater activation in the dorsolateral prefrontal cortex and the caudate in response to anticipated receipt of food but less activation in the lateral orbitofrontal cortex in response to receipt of food (false discovery rate-corrected P < .05). Similar patterns of neural activation are implicated in addictive-like eating behavior and substance dependence: elevated activation in reward circuitry in response to food cues and reduced activation of inhibitory regions in response to food intake.
    Archives of general psychiatry 04/2011; 68(8):808-16. · 12.26 Impact Factor
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    ABSTRACT: 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.
    Journal of Neuroscience 03/2011; 31(12):4360-6. · 6.91 Impact Factor
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    ABSTRACT: Data suggest that low levels of dopamine D2 receptors and attenuated responsivity of dopamine-target regions to food intake is associated with increased eating and elevated weight. There is also growing (although mixed) evidence that genotypes that appear to lead to reduced dopamine signaling (e.g., DRD2, DRD4, and DAT) and certain appetite-related hormones and peptides (e.g., ghrelin, orexin A, leptin) moderate the relation between dopamine signaling, overeating, and obesity. This chapter reviews findings from studies that have investigated the relation between dopamine functioning and food intake and how certain genotypes and appetite-related hormones and peptides affect this relation.
    Current topics in behavioral neurosciences. 01/2011; 6:81-93.
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    Laura Batterink, Sonja Yokum, Eric Stice
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    ABSTRACT: Self-report and behavioral data suggest that impulsivity may contribute to the development and maintenance of obesity. Neuroimaging studies implicate a widespread neural network in inhibitory control and suggest that impulsive individuals show hypoactivity in these regions during tasks requiring response inhibition. Yet, research has not directly tested whether body mass correlates inversely with activation of these regions during response inhibition tasks. The present study used functional magnetic resonance imaging (fMRI) to investigate neural activations during a food-specific go/no-go task in adolescent girls ranging from lean to obese. When required to inhibit prepotent responses to appetizing food, body mass index (BMI) correlated with response inhibition at both the behavioral and neural levels, with more overweight adolescents showing greater behavioral evidence of impulsivity as well as reduced activation of frontal inhibitory regions, including superior frontal gyrus, middle frontal gyrus, ventrolateral prefrontal cortex, medial prefrontal cortex, and orbitofrontal cortex, than leaner individuals. As well, activation in food reward regions (e.g., temporal operculum/insula) in response to food images correlated positively with BMI. Results suggest that hypofunctioning of inhibitory control regions and increased response of food reward regions are related to elevated weight.
    NeuroImage 10/2010; 52(4):1696-703. · 6.25 Impact Factor
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    ABSTRACT: 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.
    Journal of Neuroscience 09/2010; 30(39):13105-9. · 6.91 Impact Factor
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    ABSTRACT: This study tested the hypotheses that dietary restraint scores are associated with greater reward sensitivity and cognitive bias for food-related cues, which might result in chronic overeating and efforts to curb this tendency through dietary restriction. Participants (N=63) with high versus low scores on the DEBQ-R did not differ on attentional bias for pictorial food-related cues on a visual probe task, or approach tendencies elicited by food cues, as assessed with a stimulus-response compatibility (SRC) task. Restraint was also unrelated to performance on an operant task that assessed how hard participants would work for snacks, or responding during a taste habituation paradigm. Dietary restraint scores were correlated with self-reported appetitive response to food, sensitivity to reward, and sensitivity to punishment. Results provide limited support for the hypothesis that individuals with elevated dietary restraint scores show greater reward sensitivity and cognitive bias for food stimuli, though it is possible that the null findings on the behavioral task resulted because of an approach-avoidance conflict to food cues in which heightened appetitive responses to food are inhibited by food-related anxiety.
    Appetite 08/2010; 55(1):61-8. · 2.54 Impact Factor
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    ABSTRACT: To determine whether responsivity of reward circuitry to food predicts future increases in body mass and whether polymorphisms in DRD2 and DRD4 moderate these relations. The functional magnetic resonance imaging (fMRI) paradigm investigated blood oxygen level dependent activation in response to imagined intake of palatable foods, unpalatable foods, and glasses of water shown in pictures. DNA was extracted from saliva samples using standard salting-out and solvent precipitation methods. Forty-four adolescent female high school students ranging from lean to obese. Future increases in body mass index (BMI). Weaker activation of the frontal operculum, lateral orbitofrontal cortex, and striatum in response to imagined intake of palatable foods, versus imagined intake of unpalatable foods or water, predicted future increases in body mass for those with the DRD2 TaqIA A1 allele or the DRD4-7R allele. Data also suggest that for those lacking these alleles, greater responsivity of these food reward regions predicted future increases in body mass. This novel prospective fMRI study indicates that responsivity of reward circuitry to food increases risk for future weight gain, but that genes that impact dopamine signaling capacity moderate the predictive effects, suggesting two qualitatively distinct pathways to unhealthy weight gain based on genetic risk.
    NeuroImage 05/2010; 50(4):1618-25. · 6.25 Impact Factor