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Sarah E. Racine

Bio: Sarah E. Racine is an academic researcher from McGill University. The author has contributed to research in topics: Binge eating & Eating disorders. The author has an hindex of 21, co-authored 60 publications receiving 1583 citations. Previous affiliations of Sarah E. Racine include University of Pittsburgh & Michigan State University.


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TL;DR: Multiple biopsychosocial influences are implicated in eating disorders and/or disordered eating symptoms and several can now be considered established risk factors.
Abstract: Background Eating disorders are severe psychiatric disorders with a complex etiology involving transactions among sociocultural, psychological, and biological influences. Most research and reviews, however, focus on only one level of analysis. To address this gap, we provide a qualitative review and summary using an integrative biopsychosocial approach. Methods We selected variables for which there were available data using integrative methodologies (e.g., twin studies, gene-environment interactions) and/or data at the biological and behavioral level (e.g., neuroimaging). Factors that met these inclusion criteria were idealization of thinness, negative emotionality, perfectionism, negative urgency, inhibitory control, cognitive inflexibility, serotonin, dopamine, ovarian hormones. Literature searches were conducted using PubMed. Variables were classified as risk factors or correlates of eating disorder diagnoses and disordered eating symptoms using Kraemer et al.'s (1997) criteria. Findings Sociocultural idealization of thinness variables (media exposure, pressures for thinness, thin-ideal internalization, thinness expectancies) and personality traits (negative emotionality, perfectionism, negative urgency) attained ‘risk status’ for eating disorders and/or disordered eating symptoms. Other factors were identified as correlates of eating pathology or were not classified given limited data. Effect sizes for risk factors and correlates were generally small-to-moderate in magnitude. Conclusions Multiple biopsychosocial influences are implicated in eating disorders and/or disordered eating symptoms and several can now be considered established risk factors. Data suggest that psychological and environmental factors interact with and influence the expression of genetic risk to cause eating pathology. Additional studies that examine risk variables across multiple levels of analysis and that consider specific transactional processes amongst variables are needed to further elucidate the intersection of sociocultural, psychological, and biological influences on eating disorders.

382 citations

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TL;DR: Examining ovarian hormone interactions in the prediction of within-subject changes in emotional eating in the largest sample of women to date confirmed that changes in ovarian hormones predict changes inotional eating across the menstrual cycle, with a significant estradiol × progesterone interaction.
Abstract: Studies suggest that within-person changes in estrogen and progesterone predict changes in binge eating across the menstrual cycle. However, samples have been extremely small (maximum N = 9), and analyses have not examined the interactive effects of hormones that are critical for changes in food intake in animals. The aims of the current study were to examine ovarian hormone interactions in the prediction of within-subject changes in emotional eating in the largest sample of women to date (N = 196). Participants provided daily ratings of emotional eating and saliva samples for hormone measurement for 45 consecutive days. Results confirmed that changes in ovarian hormones predict changes in emotional eating across the menstrual cycle, with a significant estradiol × progesterone interaction. Emotional eating scores were highest during the midluteal phase, when progesterone peaks and estradiol demonstrates a secondary peak. Findings extend previous work by highlighting significant interactions between estrogen and progesterone that explain midluteal increases in emotional eating. Future work should explore mechanisms (e.g., gene-hormone interactions) that contribute to both within- and between-subjects differences in emotional eating.

162 citations

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TL;DR: Analysis of associations between specific difficulties with emotion regulation and the core symptoms of anorexia nervosa suggests that parsing the construct of emotion regulation as well as the AN phenotype can help to identify the unique ways in which eating disorder symptoms may function to regulate emotions.
Abstract: Objective Extant research suggests that individuals with anorexia nervosa (AN) have deficits in emotion regulation across a variety of domains The current study investigated associations between specific difficulties with emotion regulation and the core symptoms of AN

115 citations

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TL;DR: Examination of phenotypic and etiologic associations between negative urgency, negative affect, and dysregulated eating in a sample of 222 same-sex female twin pairs from the Michigan State University Twin Registry suggests that the presence of emotion-based rash action, combined with high levels ofnegative affect, may significantly increase genetic risk for Dysregulated eating.
Abstract: Negative urgency (i.e., the tendency to engage in rash action in response to negative affect) has emerged as a critical personality trait contributing to individual differences in binge eating. However, studies investigating the extent to which genetic and/or environmental influences underlie the effects of negative urgency on binge eating are lacking. Moreover, it remains unclear whether negative urgency-binge eating associations are simply a result of the well-established role of negative affect in the development/maintenance of binge eating. The current study addresses these gaps by examining phenotypic and etiologic associations between negative urgency, negative affect, and dysregulated eating (i.e., binge eating, emotional eating) in a sample of 222 same-sex female twin pairs from the Michigan State University Twin Registry. Negative urgency was significantly associated with both dysregulated eating symptoms, even after controlling for the effects of negative affect. Genetic factors accounted for the majority (62-77%) of this phenotypic association, although a significant proportion of this genetic covariation was due to genetic influences in common with negative affect. Nonshared environmental factors accounted for a relatively smaller (23-38%) proportion of the association, but these nonshared environmental effects were independent of negative affect. Findings suggest that the presence of emotion-based rash action, combined with high levels of negative affect, may significantly increase genetic risk for dysregulated eating.

100 citations

Journal ArticleDOI
TL;DR: Findings provide support for sex differences in rodent models of binge eating and highlight the promise of the BER/BEP model for understanding neurobiological mechanisms underlying sex Differences in risk.
Abstract: Objective Several efforts are underway to model binge eating in animals in order to advance neurobiological models of risk. However, knowledge of sex differences in these models is currently lacking. The goal of the present study was to examine sex differences in binge eating phenotypes using a well-established rodent model (i.e., the binge eating resistant/binge eating prone model). Method Thirty male and 30 female adult Sprague-Dawley rats were exposed to feeding tests consisting of intermittent access to palatable food (PF). Rats were then categorized as binge eating prone (BEP) based on the amount and consistency of PF consumption across tests. Results Across multiple methods for BEP classification, rates of BEP phenotypes were two to six times higher in female than male rats. Discussion Findings provide support for sex differences in rodent models of binge eating and highlight the promise of the BER/BEP model for understanding neurobiological mechanisms underlying sex differences in risk. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:729–736)

99 citations


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2,102 citations

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893 citations

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TL;DR: This manuscript demonstrates that the practice of improperly controlling for covariates is the norm in the G × E interaction literature to date and shows that many alternative explanations for G ×E findings that investigators had thought were eliminated have not been.

521 citations