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Objective: To assess the feasibility of engaging stressed, low-income parents with obesity in a novel mindfulness-based parent stress intervention aimed at decreasing the risk of early childhood obesity., Study Design: An 8-week mindfulness-based parent stress group intervention (parenting mindfully for health) plus nutrition and physical activity counseling (PMH+N) was developed for parents with obesity aimed at preventing obesity in their at-risk 2- to 5-year-old children. PMH+N was compared with a control group intervention (C+N), and improvement in parenting was assessed before and after the intervention using the laboratory-based toy wait task (TWT). In addition, nutrition, physical activity, and stress were assessed using a multimethod approach., Results: After establishing feasibility in 20 parent-child dyads (phase 1), 42 dyads were randomized to PMH+N vs C+N (phase 2). Compared with the C+N group, the PMH+N group demonstrated significantly better group attendance (P < .015), greater improvement in parental involvement (P < .05), and decreased parental emotional eating rating (P < .011). Furthermore, C+N, but not PMH+N, was associated with significant increases in child body mass index percentile during treatment (P < .03) when accounting for the TWT before and after changes in parenting scores., Conclusions: These findings suggest that a mindfulness-based parent stress intervention to decrease childhood obesity risk is feasible, requires further testing of therapeutic mechanisms in larger samples, and may be a potential way to attenuate the risk of childhood obesity., Trial Registration: ClinicalTrials.govNCT01974102., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Objective: Screening for depression, diabetes distress, and disordered eating in youth with type 1 diabetes (T1D) is recommended, as these comorbidities contribute to poor glycemic control. No consensus exists on which measures are optimal, and most previous studies have used nondisease-specific measures. We examined the utility of screening for these disorders using two disease-specific and one general measure at the time of transition from pediatric to adult care., Methods: Forty-three young adults from a T1D transition clinic completed the Patient Health Questionnaire, the Diabetes Distress Scale, and the Diabetes Eating Problem Survey-Revised. Chart review determined if clinicians noted similar symptoms during the year prior to transition. Metabolic data were also recorded., Results: Chart review identified 5 patients with depressive symptoms and 8 patients with diabetes distress. Screening identified 2 additional patients with depressive symptoms and 1 additional patient with diabetes distress. Of those noted to have symptomatic depression or diabetes distress on chart review, several subsequently screened negative on transition. Disordered eating was not detected by chart review, but 23.5% screened positive on transition. While depression, diabetes distress, and disordered eating positively correlated with glycated hemoglobin (HbA1c) (r = 0.31, P = .05; r = 0.40, P = .009; r = 0.63, P<.001, respectively), disordered eating accounted for the majority of observed variance (df = 1; F = 18.6; P<.001). Even though HbA1c was higher in patients with versus without disordered eating (P<.001), body mass index did not differ between the 2 groups (P = .51)., Conclusion: In young adults with T1D, formal screening provides an opportunity to detect psychological problems, which, when treated, may help optimize metabolic control during the transition process., Abbreviations: T1D = type 1 diabetes HbA1C = hemoglobin A1c YCDP = Yale Children's Diabetes Program PHQ-8 = Patient Health Questionnaire-8 DDS = Diabetes Distress Scale DEPS-R = Diabetes Eating Problem Survey-Revised.

Introduction: Tobacco-use disorder is a complex condition involving multiple brain networks and presenting with multiple behavioral correlates including changes in diet and stress. In a previous functional magnetic resonance imaging (fMRI) study of neural responses to favorite-food, stress, and neutral-relaxing imagery, smokers versus nonsmokers demonstrated blunted corticostriatal-limbic responses to favorite-food cues. Based on other recent reports of alterations in functional brain networks in smokers, the current study examined functional connectivity during exposure to favorite-food, stress, and neutral-relaxing imagery in smokers and nonsmokers, using the same dataset., Methods: The intrinsic connectivity distribution was measured to identify brain regions that differed in degree of functional connectivity between groups during each imagery condition. Resulting clusters were evaluated for seed-to-voxel connectivity to identify the specific connections that differed between groups during each imagery condition., Results: During exposure to favorite-food imagery, smokers versus nonsmokers showed lower connectivity in the supramarginal gyrus, and differences in connectivity between the supramarginal gyrus and the corticostriatal-limbic system. During exposure to neutral-relaxing imagery, smokers versus nonsmokers showed greater connectivity in the precuneus, and greater connectivity between the precuneus and the posterior insula and rolandic operculum. During exposure to stress imagery, smokers versus nonsmokers showed lower connectivity in the cerebellum., Conclusions: These findings provide data-driven insights into smoking-related alterations in brain functional connectivity patterns related to appetitive, relaxing, and stressful states., Implications: This study uses a data-driven approach to demonstrate that smokers and nonsmokers show differential patterns of functional connectivity during guided imagery related to personalized favorite-food, stress, and neutral-relaxing cues, in brain regions implicated in attention, reward-related, emotional, and motivational processes. For smokers, these differences in connectivity may impact appetite, stress, and relaxation, and may interfere with smoking cessation., (© The Author 2016. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Stress is associated with obesity, and the neurobiology of stress overlaps significantly with that of appetite and energy regulation. This review will discuss stress, allostasis, the neurobiology of stress and its overlap with neural regulation of appetite, and energy homeostasis. Stress is a key risk factor in the development of addiction and in addiction relapse. High levels of stress changes eating patterns and augments consumption of highly palatable (HP) foods, which in turn increases incentive salience of HP foods and allostatic load. The neurobiological mechanisms by which stress affects reward pathways to potentiate motivation and consumption of HP foods as well as addictive drugs is discussed. With enhanced incentive salience of HP foods and overconsumption of these foods, there are adaptations in stress and reward circuits that promote stress-related and HP food-related motivation as well as concomitant metabolic adaptations, including alterations in glucose metabolism, insulin sensitivity, and other hormones related to energy homeostasis. These metabolic changes in turn might also affect dopaminergic activity to influence food motivation and intake of HP foods. An integrative heuristic model is proposed, wherein repeated high levels of stress alter the biology of stress and appetite/energy regulation, with both components directly affecting neural mechanisms contributing to stress-induced and food cue-induced HP food motivation and engagement in overeating of such foods to enhance risk of weight gain and obesity. Future directions in research are identified to increase understanding of the mechanisms by which stress might increase risk of weight gain and obesity., (Copyright © 2013 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Objective: Obesity is associated with alterations in corticolimbic-striatal brain regions involved in food motivation and reward. Stress and the presence of food cues may each motivate eating and engage corticolimibic-striatal neurocircuitry. It is unknown how these factors interact to influence brain responses and whether these interactions are influenced by obesity, insulin levels, and insulin sensitivity. We hypothesized that obese individuals would show greater responses in corticolimbic-striatal neurocircuitry after exposure to stress and food cues and that brain activations would correlate with subjective food craving, insulin levels, and HOMA-IR., Research Design and Methods: Fasting insulin levels were assessed in obese and lean subjects who were exposed to individualized stress and favorite-food cues during functional MRI., Results: Obese, but not lean, individuals exhibited increased activation in striatal, insular, and hypothalamic regions during exposure to favorite-food and stress cues. In obese but not lean individuals, food craving, insulin, and HOMA-IR levels correlated positively with neural activity in corticolimbic-striatal brain regions during favorite-food and stress cues. The relationship between insulin resistance and food craving in obese individuals was mediated by activity in motivation-reward regions including the striatum, insula, and thalamus., Conclusions: These findings demonstrate that obese, but not lean, individuals exhibit increased corticolimbic-striatal activation in response to favorite-food and stress cues and that these brain responses mediate the relationship between HOMA-IR and food craving. Improving insulin sensitivity and in turn reducing corticolimbic-striatal reactivity to food cues and stress may diminish food craving and affect eating behavior in obesity.

Stress is associated with alterations in neural motivational-reward pathways in the ventral striatum (VS), hormonal/metabolic changes, and weight increases. The relationship between these different factors is not well understood. We hypothesized that body mass index (BMI) status and hormonal/metabolic factors would be associated with VS activation. We used functional magnetic resonance imaging (fMRI) to compare brain responses of overweight and obese (OW/OB: BMI ≥ 25 kg/m(2): N=27) individuals with normal weight (NW: BMI<18.5-24.9 kg/m(2): N=21) individuals during exposure to personalized stress, alcohol cue, and neutral-relaxing situations using a validated, autobiographical, script-driven, guided-imagery paradigm. Metabolic factors, including fasting plasma glucose (FPG), insulin, and leptin, were examined for their association with VS activation. Consistent with previous studies, stress and alcohol cue exposure each increased activity in cortico-limbic regions. Compared with NW individuals, OW/OB individuals showed greater VS activation in the neutral-relaxing and stress conditions. FPG was correlated with VS activation. Significant associations between VS activation and metabolic factors during stress and relaxation suggest the involvement of metabolic factors in striatal dysfunction in OW/OB individuals. This relationship may contribute to non-homeostatic feeding in obesity.