Cara Bohon

Relation Between Obesity and Blunted Striatal Response to Food Is Moderated by TaqIA A1 Allele

The dorsal striatum plays a role in consummatory food reward, and striatal dopamine receptors are reduced in obese individuals, relative to lean individuals, which suggests that the striatum and dopaminergic signaling in the striatum may contribute to the 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 the presence of the A1 allele of the TaqIA restriction fragment length polymorphism, which is associated with dopamine D2 receptor (DRD2) gene binding in the striatum and compromised striatal dopamine signaling. Cross-sectional and prospective data from two functional magnetic resonance imaging studies support these hypotheses, which implies that individuals may overeat to compensate for a hypofunctioning dorsal striatum, particularly those with genetic polymorphisms thought to attenuate dopamine signaling in this region.

Relation of reward from food intake and anticipated food intake to obesity: a functional magnetic resonance imaging study.

The authors 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 (mean 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 (vs. a tasteless solution) and to actual consumption of milkshake (vs. 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.

Reciprocal relations between rumination and bulimic, substance abuse, and depressive symptoms in female adolescents.

The authors examined the reciprocal relations between rumination and symptoms of depression, bulimia, and substance abuse with longitudinal data from 496 female adolescents. Rumination predicted future increases in bulimic and substance abuse symptoms, as well as onset of major depression, binge eating, and substance abuse. Depressive and bulimic, but not substance abuse, symptoms predicted increases in rumination. Rumination did not predict increases in externalizing symptoms, providing evidence for the specificity of effects of rumination, although externalizing symptoms predicted future increases in rumination. Results suggest rumination may contribute to the etiology of depressive, bulimic, and substance abuse pathology and that the former two disturbances may foster increased rumination. Results imply that it might be beneficial for prevention programs to target this cognitive vulnerability.

A Meta-Analytic Review of Depression Prevention Programs for Children and Adolescents: Factors that Predict Magnitude of Intervention Effects

In this meta-analytic review, the authors summarized the effects of depression prevention programs for youth as well as investigated participant, intervention, provider, and research design features associated with larger effects. They identified 47 trials that evaluated 32 prevention programs, producing 60 intervention effect sizes. The average effect for depressive symptoms from pre-to-posttreatment (r = .15) and pretreatment to-follow-up (r = .11) were small, but 13 (41%) prevention programs produced significant reductions in depressive symptoms and 4 (13%) produced significant reductions in risk for future depressive disorder onset relative to control groups. Larger effects emerged for programs targeting high-risk individuals, samples with more females, samples with older adolescents, programs with a shorter duration and with homework assignments, and programs delivered by professional interventionists. Intervention content (e.g., a focus on problem-solving training or reducing negative cognitions) and design features (e.g., use of random assignment and structured interviews) were unrelated to effect sizes. Results suggest that depression prevention efforts produce a higher yield if they incorporate factors associated with larger intervention effects (e.g., selective programs with a shorter duration that include homework).

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.

Reward circuitry responsivity to food predicts future increases in body mass: moderating effects of DRD2 and DRD4.

OBJECTIVE 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. DESIGN 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. PARTICIPANTS Forty-four adolescent female high school students ranging from lean to obese. MAIN OUTCOME Future increases in body mass index (BMI). RESULTS 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. DISCUSSION 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.

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.

Reward abnormalities among women with full and subthreshold bulimia nervosa: A functional magnetic resonance imaging study

OBJECTIVE To test the hypothesis that women with full and subthreshold bulimia nervosa show abnormal neural activation in response to food intake and anticipated food intake relative to healthy control women. METHOD Females with and without full/subthreshold bulimia nervosa recruited from the community (N = 26) underwent functional magnetic resonance imaging (fMRI) during receipt and anticipated receipt of chocolate milkshake and a tasteless control solution. RESULTS Women with bulimia nervosa showed trends for less activation than healthy controls in the right anterior insula in response to anticipated receipt of chocolate milkshake (vs. tasteless solution) and in the left middle frontal gyrus, right posterior insula, right precentral gyrus, and right mid dorsal insula in response to consumptions of milkshake (vs. tasteless solution). DISCUSSION Bulimia nervosa may be related to potential hypofunctioning of the brain reward system, which may lead these individuals to binge eat to compensate for this reward deficit, though the hypo-responsivity might be a result of a history of binge eating highly palatable foods.

Female emotional eaters show abnormalities in consummatory and anticipatory food reward: a functional magnetic resonance imaging study.

OBJECTIVE To test the hypothesis that emotional eaters show greater neural activation in response to food intake and anticipated food intake than nonemotional eaters and whether these differences are amplified during a negative versus neutral mood state. METHOD Female emotional eaters and nonemotional eaters (N = 21) underwent functional magnetic resonance imaging (fMRI) during receipt and anticipated receipt of chocolate milkshake and a tasteless control solution while in a negative and neutral mood. RESULTS Emotional eaters showed greater activation in the parahippocampal gyrus and anterior cingulate (ACC) in response to anticipated receipt of milkshake and greater activation in the pallidum, thalamus, and ACC in response to receipt of milkshake during a negative relative to a neutral mood. In contrast, nonemotional eaters showed decreased activation in reward regions during a negative versus a neutral mood. DISCUSSION Results suggest that emotional eating is related to increased anticipatory and consummatory food reward, but only during negative mood.

Subtyping Women with Bulimia Nervosa Along Dietary and Negative Affect Dimensions: Further Evidence of Reliability and Validity

Studies have found that individuals with bulimia nervosa can be classified into dietary and dietary-negative affect subtypes and that the latter exhibit greater eating pathology, psychiatric comorbidity, and functional impairment; a more protracted clinical course; and a worse treatment response. In this report, the authors describe 2 prospective studies that found that young women with threshold (n = 48) and subthreshold (n = 83) bulimic pathology can be classified into dietary and dietary-negative affect subtypes; that two subtyping approaches produced similar results (mean kappa = .94); that the subtyping distinction showed 4-week test-retest reliability (kappa = .61); and that the dietary-negative affect subtype showed greater eating pathology, emotional distress, functional impairment, treatment seeking, and lower likelihood of recovery over 6-month and 3-year follow-ups than the dietary subtype. The dieting-negative affect subtyping distinction evidenced greater test-retest reliability and concurrent and predictive validity than did the purging-nonpurging subtyping distinction. The additional evidence for the reliability and validity of this subtyping scheme, particularly the prognostic utility, suggests it is worth additional inquiry.