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1.
Int J Eat Disord ; 57(7): 1433-1446, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38650547

RESUMO

OBJECTIVE: Binge-eating disorder is an eating disorder characterized by recurrent binge-eating episodes, during which individuals consume excessive amounts of highly palatable food (HPF) in a short time. This study investigates the intricate relationship between repeated binge-eating episode and the transcriptional regulation of two key genes, adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R), in selected brain regions of rats. METHOD: Binge-like eating behavior on HPF was induced through the combination of food restrictions and frustration stress (15 min exposure to HPF without access to it) in female rats, compared to control rats subjected to only restriction or only stress or none of these two conditions. After chronic binge-eating episodes, nucleic acids were extracted from different brain regions, and gene expression levels were assessed through real-time quantitative PCR. The methylation pattern on genes' promoters was investigated using pyrosequencing. RESULTS: The analysis revealed A2AAR upregulation in the amygdala and in the ventral tegmental area (VTA), and D2R downregulation in the nucleus accumbens in binge-eating rats. Concurrently, site-specific DNA methylation alterations at gene promoters were identified in the VTA for A2AAR and in the amygdala and caudate putamen for D2R. DISCUSSION: The alterations on A2AAR and D2R genes regulation highlight the significance of epigenetic mechanisms in the etiology of binge-eating behavior, and underscore the potential for targeted therapeutic interventions, to prevent the development of this maladaptive feeding behavior. These findings provide valuable insights for future research in the field of eating disorders. PUBLIC SIGNIFICANCE: Using an animal model with face, construct, and predictive validity, in which cycles of food restriction and frustration stress evoke binge-eating behavior, we highlight the significance of epigenetic mechanisms on adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R) genes regulation. They could represent new potential targets for the pharmacological management of eating disorders characterized by this maladaptive feeding behavior.


Assuntos
Transtorno da Compulsão Alimentar , Bulimia , Receptor A2A de Adenosina , Receptores de Dopamina D2 , Recompensa , Animais , Receptores de Dopamina D2/metabolismo , Receptores de Dopamina D2/genética , Feminino , Ratos , Receptor A2A de Adenosina/genética , Receptor A2A de Adenosina/metabolismo , Bulimia/metabolismo , Bulimia/genética , Transtorno da Compulsão Alimentar/genética , Transtorno da Compulsão Alimentar/metabolismo , Encéfalo/metabolismo , Modelos Animais de Doenças , Regulação da Expressão Gênica , Metilação de DNA , Área Tegmentar Ventral/metabolismo , Comportamento Alimentar , Núcleo Accumbens/metabolismo , Ratos Sprague-Dawley
2.
Proc Natl Acad Sci U S A ; 118(13)2021 03 30.
Artigo em Inglês | MEDLINE | ID: mdl-33753517

RESUMO

Leptin-deficient ob/ob mice eat voraciously, and their food intake is markedly reduced by leptin treatment. In order to identify potentially novel sites of leptin action, we used PhosphoTRAP to molecularly profile leptin-responsive neurons in the hypothalamus and brainstem. In addition to identifying several known leptin responsive populations, we found that neurons in the dorsomedial hypothalamus (DMH) of ob/ob mice expressing protein phosphatase 1 regulatory subunit 17 (PPP1R17) constitutively express cFos and that this is suppressed by leptin treatment. Because ob mice are hyperphagic, we hypothesized that activating PPP1R17 neurons would increase food intake. However, chemogenetic activation of PPP1R17 neurons decreased food intake and body weight of ob/ob mice while inhibition of PPP1R17 neurons increased them. Similarly, in a scheduled feeding protocol that elicits increased consumption, mice also ate more when PPP1R17 neurons were inhibited and ate less when they were activated. Finally, we found that pair-feeding of ob mice reduced cFos expression to a similar extent as leptin and that reducing the amount of food available during scheduled feeding in DMHPpp1r17 neurons also decreased cFos in DMHPpp1r17 neurons. Finally, these neurons do not express the leptin receptor, suggesting that the effect of leptin on these neurons is indirect and secondary to reduced food intake. In aggregate, these results show that PPP1R17 neurons in the DMH are activated by increased food intake and in turn restrict intake to limit overconsumption, suggesting that they function to constrain binges of eating.


Assuntos
Bulimia/fisiopatologia , Núcleo Hipotalâmico Dorsomedial/fisiopatologia , Ingestão de Alimentos/fisiologia , Leptina/fisiologia , Inibição Neural , Neurônios/fisiologia , Proteínas/metabolismo , Animais , Bulimia/genética , Núcleo Hipotalâmico Dorsomedial/efeitos dos fármacos , Núcleo Hipotalâmico Dorsomedial/metabolismo , Ingestão de Alimentos/genética , Leptina/genética , Leptina/farmacologia , Camundongos , Camundongos Obesos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Proteínas/genética , Proteínas Proto-Oncogênicas c-fos/metabolismo , Resposta de Saciedade
3.
Behav Genet ; 53(2): 143-153, 2023 03.
Artigo em Inglês | MEDLINE | ID: mdl-36484893

RESUMO

Although bivariate associations between attention-deficit/hyperactivity disorder (ADHD) and eating disorders in adolescent girls and boys have been previously identified, the mechanistic link underlying the symptom-level associations remains unclear. We evaluated shared genetic and environmental influences on ADHD symptoms and disordered eating in 819 female and 756 male twins from the Swedish TCHAD cohort using bivariate models. Common additive genetic and unique environmental effects accounted for majority of ADHD and disordered eating associations in a differential manner. For girls, the strongest genetic correlation was observed for cognitive/inattention problems-bulimia (0.54), with genetic factors accounting for 67% of the phenotypic correlation. For boys, the strongest genetic correlations were observed for conduct problems-bulimia and hyperactivity-bulimia (~ 0.54), accounting for 83% and 95% of the phenotypic correlation, respectively. As per our findings, the risk of comorbidity and shared genetics highlights the need for preventative measures and specialized treatment for ADHD and disordered eating in both sexes.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade , Bulimia , Transtornos da Alimentação e da Ingestão de Alimentos , Humanos , Masculino , Adolescente , Feminino , Transtorno do Deficit de Atenção com Hiperatividade/genética , Bulimia/complicações , Bulimia/genética , Gêmeos/genética , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Transtornos da Alimentação e da Ingestão de Alimentos/complicações , Comorbidade
4.
Am J Physiol Endocrinol Metab ; 322(6): E494-E507, 2022 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-35403437

RESUMO

Binge-eating disorder is the most prevalent eating disorder diagnosed, affecting three times more women than men. Ghrelin stimulates appetite and reward signaling, and loss of its receptor reduces binge-eating behavior in male mice. Here, we examined the influence of ghrelin itself on binge-eating behavior in both male and female mice. Five-wk-old wild-type (WT) and ghrelin-deficient (Ghrl-/-) mice were housed individually in indirect calorimetry cages for 9 wks. Binge-like eating was induced by giving mice ad libitum chow, but time-restricted access to a Western-style diet (WD; 2 h access, 3 days/wk) in the light phase (BE); control groups received ad libitum chow (CO), or ad libitum access to both diets (CW). All groups of BE mice showed binge-eating behavior, eating up to 60% of their 24-h intake during the WD access period. Subsequent dark phase chow intake was decreased in Ghrl-/- mice and remained decreased in Ghrl-/- females on nonbinge days. Also, nonbinge day locomotor activity was lower in Ghrl-/- than in WT BE females. Upon euthanasia, Ghrl-/- BE mice weighed less and had a lower lean body mass percentage than WT BE mice. In BE and CW groups, ghrelin and sex altered the expression of genes involved in lipid processing, thermogenesis, and aging in white adipose tissue and livers. We conclude that, although ghrelin deficiency does not hamper the development of binge-like eating, it sex-dependently alters food intake timing, locomotor activity, and metabolism. These results add to the growing body of evidence that ghrelin signaling is sexually dimorphic.NEW & NOTEWORTHY Ghrelin, a peptide hormone secreted from the gut, is involved in hunger and reward signaling, which are altered in binge-eating disorder. Although sex differences have been described in both binge-eating and ghrelin signaling, this interaction has not been fully elucidated. Here, we show that ghrelin deficiency affects the behavior and metabolism of mice in a binge-like eating paradigm, and that the sex of the mice impacts the magnitude and direction of these effects.


Assuntos
Transtorno da Compulsão Alimentar , Bulimia , Animais , Bulimia/genética , Bulimia/metabolismo , Modelos Animais de Doenças , Ingestão de Alimentos/genética , Comportamento Alimentar , Feminino , Expressão Gênica , Grelina/metabolismo , Fígado/metabolismo , Locomoção , Masculino , Camundongos
5.
BMC Psychiatry ; 20(1): 307, 2020 06 16.
Artigo em Inglês | MEDLINE | ID: mdl-32546136

RESUMO

BACKGROUND: The Binge Eating Genetics Initiative (BEGIN) is a multipronged investigation examining the interplay of genomic, gut microbiota, and behavioral factors in bulimia nervosa and binge-eating disorder. METHODS: 1000 individuals who meet current diagnostic criteria for bulimia nervosa or binge-eating disorder are being recruited to collect saliva samples for genotyping, fecal sampling for microbiota characterization, and recording of 30 days of passive data and behavioral phenotyping related to eating disorders using the app Recovery Record adapted for the Apple Watch. DISCUSSION: BEGIN examines the interplay of genomic, gut microbiota, and behavioral factors to explore etiology and develop predictors of risk, course of illness, and response to treatment in bulimia nervosa and binge-eating disorder. We will optimize the richness and longitudinal structure of deep passive and active phenotypic data to lay the foundation for a personalized precision medicine approach enabling just-in-time interventions that will allow individuals to disrupt eating disorder behaviors in real time before they occur. TRIAL REGISTRATION: The ClinicalTrials.gov identifier is NCT04162574. November 14, 2019, Retrospectively Registered.


Assuntos
Transtorno da Compulsão Alimentar , Bulimia Nervosa , Bulimia , Transtornos da Alimentação e da Ingestão de Alimentos , Transtorno da Compulsão Alimentar/genética , Bulimia/genética , Bulimia Nervosa/genética , Comportamento Alimentar , Humanos
6.
Eur J Neurosci ; 50(3): 2430-2445, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-30667547

RESUMO

Many eating-related psychological constructs have been proposed to explain obesity and overeating. However, these constructs, including food addiction, disinhibition, hedonic hunger, emotional eating, binge eating and the like all have similar definitions, emphasizing loss of control over intake. As questionnaires measuring the constructs correlate strongly (r > 0.5) with each other, we propose that these constructs should be reconsidered to be part of a single broad phenotype: uncontrolled eating. Such an approach enables reviewing and meta-analysing evidence obtained with each individual questionnaire. Here, we describe robust associations between uncontrolled eating, body mass index (BMI), food intake, personality traits and brain systems. Reviewing cross-sectional and longitudinal data, we show that uncontrolled eating is phenotypically and genetically intertwined with BMI and food intake. We also review evidence on how three psychological constructs are linked with uncontrolled eating: lower cognitive control, higher negative affect and a curvilinear association with reward sensitivity. Uncontrolled eating mediates all three constructs' associations with BMI and food intake. Finally, we review and meta-analyse brain systems possibly subserving uncontrolled eating: namely, (i) the dopamine mesolimbic circuit associated with reward sensitivity, (ii) frontal cognitive networks sustaining dietary self-control and (iii) the hypothalamus-pituitary-adrenal axis, amygdala and hippocampus supporting stress reactivity. While there are limits to the explanatory and predictive power of the uncontrolled eating phenotype, we conclude that treating different eating-related constructs as a single concept, uncontrolled eating, enables drawing robust conclusions on the relationship between food intake and BMI, psychological variables and brain structure and function.


Assuntos
Encéfalo/diagnóstico por imagem , Bulimia/diagnóstico por imagem , Hiperfagia/diagnóstico por imagem , Obesidade/diagnóstico por imagem , Personalidade , Característica Quantitativa Herdável , Peso Corporal/fisiologia , Bulimia/genética , Bulimia/psicologia , Humanos , Hiperfagia/genética , Hiperfagia/psicologia , Obesidade/genética , Obesidade/psicologia , Personalidade/fisiologia
7.
Eat Weight Disord ; 24(5): 799-814, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31119586

RESUMO

PURPOSE: To evaluate and understand the genetic and epigenetic basis of bulimia nervosa/bulimia spectrum disorder and comorbid borderline personality disorder (BN/BSD-BPD). METHODS: The present systematic review was conducted in accordance to PRISMA guidelines. Advanced systematic searches of Medline, EMBASE, PsychINFO, Web of Science, Scopus, CINHAL plus, and the Cochrane Library were conducted using the search terms 'bulimia nervosa', 'bulimia spectrum disorder', 'borderline personality disorder', 'genes', and 'genetics'. The search strategy garnered seven studies for inclusion in the present review. RESULTS: Women with BN/BSD-BPD had significantly lower serotonin and monoamine oxidise activity compared to women with BN/BSD or healthy controls (HC). As well, women with BN/BSD-BPD displayed elevated methylation of the dopamine receptor gene promoter, brain-derived neurotrophic factor, and changes in the methylation of the glucocorticoid receptor gene promoter (NR3C1) compared to women with BN/BSD and HC. The results also demonstrated that rates of childhood sexual abuse and childhood physical abuse are higher in those with BN/BSD-BPD than those with BN/BSD and HC, and that these types of abuse are often correlated with the methylation differences seen in BN/BSD-BPD women. CONCLUSION: Due to the differences observed between individuals with BN/BSD-BPD and those with BN/BSD and HC a genetic/epigenetic aetiological model of BN/BSD-BPD was developed and is proposed in this review. This evidence-based model visually illustrates the current state of the field and draws attention to the need for subsequent research.


Assuntos
Sobreviventes Adultos de Maus-Tratos Infantis , Transtorno da Personalidade Borderline/genética , Bulimia Nervosa/genética , Bulimia/genética , Epigênese Genética , Sobreviventes Adultos de Maus-Tratos Infantis/psicologia , Transtorno da Personalidade Borderline/complicações , Transtorno da Personalidade Borderline/psicologia , Bulimia/complicações , Bulimia/psicologia , Bulimia Nervosa/complicações , Bulimia Nervosa/psicologia , Humanos
8.
Alcohol Clin Exp Res ; 42(11): 2214-2223, 2018 11.
Artigo em Inglês | MEDLINE | ID: mdl-30252141

RESUMO

BACKGROUND: Alcohol involvement has familial associations with bulimic symptoms (i.e., binge eating, inappropriate compensatory behaviors), with several studies indicating a genetic overlap between the two. It is unclear whether overlapping familial risk with alcohol involvement extends to other eating disorder symptoms. Understanding the genetic overlap between alcohol involvement and other eating disorder symptoms may aid in more targeted interventions for comorbid alcohol use-eating disorder symptoms. Thus, we investigated associations between alcohol involvement and 2 core eating disorder symptoms: drive for thinness and body dissatisfaction in adolescent female and male twins. METHODS: We assessed 3 levels of alcohol involvement: alcohol use in the last month, having ever been intoxicated, and alcohol intoxication frequency via self-report. The Eating Disorder Inventory-II assessed drive for thinness and body dissatisfaction. Sex-specific biometrical twin modeling examined the genetic overlap between alcohol involvement and eating disorder symptoms. RESULTS: Phenotypic associations between alcohol involvement, drive for thinness, and body dissatisfaction were significantly greater in girls compared with boys. A majority of the associations between alcohol involvement, drive for thinness, and body dissatisfaction in girls, but not boys, met our threshold for twin modeling (phenotypic r > 0.20). Moderate genetic correlations were observed between the 3 aspects of alcohol involvement and drive for thinness. Moderate genetic correlations were observed between alcohol use and intoxication frequency and body dissatisfaction. CONCLUSIONS: Together with the literature on alcohol involvement and bulimic symptoms, these findings suggest a generalized association between alcohol involvement and eating disorder symptoms in girls, whereas this association may be symptom specific in boys. Genetic correlations indicate that the amount and direction of this genetic overlap differs across specific symptoms. When intervening on comorbid alcohol involvement and eating disorder symptoms, it may be important to target-specific eating disorder symptoms.


Assuntos
Transtornos Relacionados ao Uso de Álcool/psicologia , Transtornos Dismórficos Corporais/psicologia , Transtornos da Alimentação e da Ingestão de Alimentos/psicologia , Magreza , Adolescente , Consumo de Bebidas Alcoólicas/genética , Consumo de Bebidas Alcoólicas/psicologia , Transtornos Relacionados ao Uso de Álcool/complicações , Transtornos Relacionados ao Uso de Álcool/genética , Intoxicação Alcoólica/genética , Intoxicação Alcoólica/psicologia , Animais , Transtornos Dismórficos Corporais/complicações , Transtornos Dismórficos Corporais/genética , Imagem Corporal , Bulimia/complicações , Bulimia/genética , Bulimia/psicologia , Transtornos da Alimentação e da Ingestão de Alimentos/complicações , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Feminino , Humanos , Masculino , Fatores Sexuais , Gêmeos
9.
Psychol Med ; 47(16): 2866-2878, 2017 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-28578734

RESUMO

BACKGROUND: Prior research demonstrated that attention-deficit hyperactivity disorder (ADHD) is associated with binge-eating behavior, binge-eating disorder (BED), and bulimia nervosa (BN). The aim of this study was to investigate these associations in an adult twin population, and to determine the extent to which ADHD symptoms and binge-eating behavior share genetic and environmental factors. METHODS: We used self-reports of current ADHD symptoms and lifetime binge-eating behavior and associated characteristics from a sample of over 18 000 adult twins aged 20-46 years, from the population-based Swedish Twin Registry. Mixed-effects logistic regression was used to examine the association between ADHD and lifetime binge-eating behavior, BED, and BN. Structural equation modeling was used in 13 773 female twins to determine the relative contribution of genetic and environmental factors to the association between ADHD symptoms and binge-eating behavior in female adult twins. RESULTS: ADHD symptoms were significantly associated with lifetime binge-eating behavior, BED, and BN. The heritability estimate for current ADHD symptoms was 0.42 [95% confidence interval (CI) 0.41-0.44], and for lifetime binge-eating behavior 0.65 (95% CI 0.54-0.74). The genetic correlation was estimated as 0.35 (95% CI 0.25-0.46) and the covariance between ADHD and binge-eating behavior was primarily explained by genetic factors (91%). Non-shared environmental factors explained the remaining part of the covariance. CONCLUSIONS: The association between adult ADHD symptoms and binge-eating behavior in females is largely explained by shared genetic risk factors.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/etiologia , Transtorno da Compulsão Alimentar/etiologia , Bulimia/etiologia , Sistema de Registros , Adulto , Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia , Transtorno do Deficit de Atenção com Hiperatividade/genética , Transtorno da Compulsão Alimentar/epidemiologia , Transtorno da Compulsão Alimentar/genética , Bulimia/epidemiologia , Bulimia/genética , Comorbidade , Suscetibilidade a Doenças , Meio Ambiente , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Suécia/epidemiologia , Adulto Jovem
10.
Int J Eat Disord ; 50(2): 157-161, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27636116

RESUMO

OBJECTIVE: Prior twin studies provide support for a single "common factor" that contributes genetic and environmental risk to a range of disordered eating symptoms. However, the common factor may be indexed less well by binge eating (BE) than other symptoms of eating disorders [i.e., body dissatisfaction (BD) and weight preoccupation (WP)]. We sought to explore the presence of a common factor and test whether loadings differed across three key symptoms (i.e., BE, BD, WP). METHOD: Disordered eating was assessed via self-report in 631 female twin pairs from the Michigan State University Twin Registry. RESULTS: We detected a common disordered eating factor that was influenced primarily by additive genetic and nonshared environmental influences. However, we observed different loadings on this common factor by symptom type, as factor loadings for BD and WP were stronger than that for BE. Moreover, the residual environmental and/or genetic variances (i.e., those that are independent of the common factor) were larger in BE than those of BD or WP. DISCUSSION: Although all three symptoms share a common set of genetic and environmental influences, risk for BE may involve additional genetic, biological, and environmental factors that are not shared with other symptoms of eating pathology. © 2016 Wiley Periodicals, Inc.(Int J Eat Disord 2017; 50:157-161).


Assuntos
Transtorno da Compulsão Alimentar/psicologia , Transtornos Dismórficos Corporais/psicologia , Imagem Corporal/psicologia , Meio Ambiente , Interação Gene-Ambiente , Adolescente , Adulto , Transtorno da Compulsão Alimentar/genética , Transtornos Dismórficos Corporais/genética , Peso Corporal/genética , Bulimia/genética , Bulimia/psicologia , Criança , Doenças em Gêmeos/genética , Emoções , Feminino , Humanos , Michigan , Sistema de Registros , Autorrelato , Meio Social , Gêmeos/genética , Adulto Jovem
11.
Eur Eat Disord Rev ; 25(5): 381-388, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28695573

RESUMO

This study examined whether self-reported and observationally measured parental behaviours were associated with disordered eating, and investigated possible moderation by a serotonin-transporter polymorphism (5-HTTLPR). Study 1 included 650 adolescents from the Australian Temperament Project who completed the Eating Disorder Inventory-2 Drive for Thinness and Bulimia scales at 15/16 years and were genotyped for 5-HTTLPR. Parents completed an Australian Temperament Project-devised measure of parental warmth and harsh punishment. Study 2 included a subgroup of 304 participants who also engaged in a video-recorded family interaction, with observed parental warmth and hostility coded by the Iowa Family Interaction Rating Scale. Greater self-reported parental warmth was associated with lower bulimia scores. Conversely, observationally measured parental warmth was associated with lower drive for thinness, but not bulimia. Self-reported parental harsh punishment was associated with bulimia only, with observed parental hostility associated with neither outcome. 5-HTTLPR genotype did not moderate the relationship between parent behaviours and adolescent disordered eating. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.


Assuntos
Comportamento do Adolescente , Atitude Frente a Saúde , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Transtornos da Alimentação e da Ingestão de Alimentos/psicologia , Poder Familiar/psicologia , Polimorfismo Genético , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Adolescente , Austrália , Bulimia/genética , Bulimia/psicologia , Impulso (Psicologia) , Feminino , Genótipo , Humanos , Masculino , Autorrelato , Temperamento , Magreza/psicologia
12.
Eur Eat Disord Rev ; 25(3): 195-204, 2017 05.
Artigo em Inglês | MEDLINE | ID: mdl-28402067

RESUMO

Altered reward reactivity is a potential risk endophenotype for eating disorders (EDs). The aim of this study was to examine reward reactivity in female twins with EDs and compare it with a twin control group. A sample of 112 twins [n = 51 met lifetime DSM-IV ED criteria (anorexia nervosa n = 26; bulimic disorders n = 24), n = 19 unaffected cotwins and n = 42 control twins] was administered measures assessing reward reactivity, including the Game of Dice Task, the Behavioural Inhibition/Activation (BIS/BAS) Scales and the Appetitive Motivation Scale (AMS). Within pair, correlations for monozygotic and dizygotic twins were calculated and generalised estimating equations compared probands with non-ED cotwins and controls. The BAS and the AMS were reduced in EDs and negatively associated with restrictive symptoms. In addition, monozygotic twins pairs demonstrated significant within pair similarity for the BAS and AMS. Conversely, there was less evidence to support the BIS or risky decision-making as measured by the Game of Dice Task as an endophenotype in EDs. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.


Assuntos
Anorexia Nervosa/psicologia , Bulimia/psicologia , Doenças em Gêmeos/psicologia , Endofenótipos , Motivação , Recompensa , Gêmeos/psicologia , Adolescente , Adulto , Anorexia Nervosa/genética , Bulimia/genética , Estudos de Casos e Controles , Doenças em Gêmeos/genética , Feminino , Humanos , Pessoa de Meia-Idade , Projetos Piloto , Fatores de Risco , Gêmeos/genética , Gêmeos/estatística & dados numéricos , Adulto Jovem
13.
Eur Eat Disord Rev ; 24(2): 91-100, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26663753

RESUMO

Eating disorders (EDs) and substance use disorders (SUDs) frequently co-occur; however, the reasons for this are unclear. We review the current literature on genetic risk for EDs and SUDs, as well as preliminary findings exploring whether these classes of disorders have overlapping genetic risk. Overall, genetic factors contribute to individual differences in liability to multiple EDs and SUDs. Although initial family studies concluded that no shared familial (which includes genetic) risk between EDs and SUDs exists, twin studies suggest a moderate proportion of shared variance is attributable to overlapping genetic factors, particularly for those EDs characterized by binge eating and/or inappropriate compensatory behaviours. No adoption or molecular genetic studies have examined shared genetic risk between these classes of disorders. Research investigating binge eating and inappropriate compensatory behaviours using emerging statistical genetic methods, as well as examining gene-environment interplay, will provide important clues into the aetiology of comorbid EDs and SUDs.


Assuntos
Transtornos da Alimentação e da Ingestão de Alimentos/genética , Predisposição Genética para Doença , Transtornos Relacionados ao Uso de Substâncias/genética , Bulimia/epidemiologia , Bulimia/genética , Comorbidade , Comportamento Alimentar/psicologia , Transtornos da Alimentação e da Ingestão de Alimentos/epidemiologia , Humanos , Fatores de Risco , Transtornos Relacionados ao Uso de Substâncias/epidemiologia
14.
Psychol Med ; 45(15): 3227-37, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-26174083

RESUMO

BACKGROUND: Previous studies have shown significant within-person changes in binge eating and emotional eating across the menstrual cycle, with substantial increases in both phenotypes during post-ovulation. Increases in both estradiol and progesterone levels appear to account for these changes in phenotypic risk, possibly via increases in genetic effects. However, to date, no study has examined changes in genetic risk for binge phenotypes (or any other phenotype) across the menstrual cycle. The goal of the present study was to examine within-person changes in genetic risk for emotional eating scores across the menstrual cycle. METHOD: Participants were 230 female twin pairs (460 twins) from the Michigan State University Twin Registry who completed daily measures of emotional eating for 45 consecutive days. Menstrual cycle phase was coded based on dates of menstrual bleeding and daily ovarian hormone levels. RESULTS: Findings revealed important shifts in genetic and environmental influences, where estimates of genetic influences were two times higher in post- as compared with pre-ovulation. Surprisingly, pre-ovulation was marked by a predominance of environmental influences, including shared environmental effects which have not been previously detected for binge eating phenotypes in adulthood. CONCLUSIONS: Our study was the first to examine within-person shifts in genetic and environmental influences on a behavioral phenotype across the menstrual cycle. Results highlight a potentially critical role for these shifts in risk for emotional eating across the menstrual cycle and underscore the need for additional, large-scale studies to identify the genetic and environmental factors contributing to menstrual cycle effects.


Assuntos
Emoções/fisiologia , Comportamento Alimentar/fisiologia , Transtornos da Alimentação e da Ingestão de Alimentos , Ciclo Menstrual/metabolismo , Sistema de Registros , Adolescente , Adulto , Bulimia/etiologia , Bulimia/genética , Bulimia/metabolismo , Meio Ambiente , Transtornos da Alimentação e da Ingestão de Alimentos/etiologia , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Transtornos da Alimentação e da Ingestão de Alimentos/metabolismo , Feminino , Predisposição Genética para Doença , Humanos , Estudos Longitudinais , Adulto Jovem
15.
Neurocase ; 21(5): 543-7, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-25158292

RESUMO

An expanded hexanucleotide (GGGGCC) repeat in a non-coding promoter region of open reading frame 72 of chromosome 9 (C9ORF72) has been recently identified as a major cause of familial and sporadic frontotemporal lobar degeneration. We describe the clinical picture of a 64-year-old woman carrying the hexanucleotide repeat expansion, who developed a sporadic early-onset form of behavioral variant frontotemporal dementia characterized by the occurrence of uncommon behavioral manifestations such as binge eating disturbance and by a rapid worsening of cognitive abilities. Our report confirms previous studies asserting that C9ORF72 repeats may sustain heterogeneous clinical syndromes.


Assuntos
Bulimia/complicações , Demência Frontotemporal/diagnóstico , Demência Frontotemporal/genética , Proteínas/genética , Encéfalo/patologia , Bulimia/genética , Proteína C9orf72 , Cognição , Expansão das Repetições de DNA , Feminino , Demência Frontotemporal/complicações , Demência Frontotemporal/psicologia , Humanos , Pessoa de Meia-Idade , Regiões Promotoras Genéticas
16.
Epidemiol Prev ; 39(5-6): 350-9, 2015.
Artigo em Italiano | MEDLINE | ID: mdl-26554686

RESUMO

This review includes relevant twin studies conducted on eating habits and preferences, and on endophenotypes of disordered eating behaviour in general population, non-clinical settings. The twin study design is presented, along with its assumptions and possible applications in aetiological and public health epidemiology. Subsequently, the strategy for the search of the scientific literature and the exclusion criteria are reported. Then, the analysis of the studies included in this review is performed, with a brief description of targeted outcomes, twin model used, sample characteristics and findings. Finally, key messages emerging from the review are highlighted, emphasizing their value for bridging the current gaps in the understanding of determinants of eating behaviour and their mode of action.


Assuntos
Ingestão de Alimentos/genética , Comportamento Alimentar , Transtornos da Alimentação e da Ingestão de Alimentos/genética , Preferências Alimentares , Anorexia/genética , Bulimia/genética , Ingestão de Alimentos/psicologia , Comportamento Alimentar/psicologia , Transtornos da Alimentação e da Ingestão de Alimentos/epidemiologia , Preferências Alimentares/psicologia , Ligação Genética , Humanos , Itália/epidemiologia , Meio Social , Estudos em Gêmeos como Assunto
17.
Int J Obes (Lond) ; 37(8): 1027-35, 2013 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-23147118

RESUMO

Melanocortin-4 receptor (MC4R) mutations are the most common known cause of monogenic obesity and an important contributor to polygenic obesity. MC4R mutations with partial or total loss of function, as well as the variant rs17782313 mapped near MC4R, are positively associated with obesity. MC4R is involved in the leptin-melanocortin signalling system, located in hypothalamic nuclei, that controls food intake via both anorexigenic or orexigenic signals. Impairment in this receptor might affect eating behaviours. Thus, in the case of MC4R mutation carriers, obesity could be related, at least partly, to inadequate control over eating behaviours. Many published studies address eating behaviours in MC4R mutation carriers. Most studies focus on binge eating disorder, whereas others examine various aspects of intake and motivation. Up to now, no evaluation of this literature has been performed. In this review, we examine the available literature on eating behaviours in carriers of MC4R mutations and variant rs17782313 near MC4R gene. We address binge eating disorder, bulimia nervosa, mealtime hyperphagia, snacking, psychological factors, satiety responsiveness and intake of energy and macro/micronutrient. In a small number of studies, MC4R mutations seem to impair eating behaviours or motivation, but no clear causal effects can be found in the balance of the evidence presented. Improvements in methodologies will be necessary to clarify the behavioural effects of MC4R mutations.


Assuntos
Bulimia/genética , Ingestão de Alimentos/genética , Comportamento Alimentar , Hiperfagia/genética , Obesidade/genética , Receptor Tipo 4 de Melanocortina/genética , Índice de Massa Corporal , Ingestão de Alimentos/psicologia , Feminino , Humanos , Leptina/genética , Masculino , Mutação/genética , Obesidade/psicologia , Fenótipo , Período Pós-Prandial , Receptor Tipo 4 de Melanocortina/metabolismo , Receptores de Superfície Celular/genética , Receptores de Superfície Celular/metabolismo
18.
Duodecim ; 129(20): 2126-32, 2013.
Artigo em Fi | MEDLINE | ID: mdl-24340712

RESUMO

Most twin studies suggest a heritability of SO to 80% for liability to eating disorders. At least moderate heritability is further supported by family and adoption studies. Polymorphisms of the 5-HT2A and BDNF genes appear robust candidates for anorexia nervosa and bulimia nervosa, while linkage studies suggest loci for anorexia nervosa in chromosome 1 and a locus in chromosome 10 for bulimia nervosa. Contemporary Western culture has a salient role in the rising incidence of eating disorders, and epigenetic mechanisms are suggested to be involved. In the near future, GWAS will likely provide compelling new data of genetic etiology and mechanisms of eating disorders.


Assuntos
Transtornos da Alimentação e da Ingestão de Alimentos/genética , Predisposição Genética para Doença , Anorexia/genética , Fator Neurotrófico Derivado do Encéfalo/genética , Bulimia/genética , Cromossomos Humanos Par 1 , Cromossomos Humanos Par 10 , Características Culturais , Epigenômica , Ligação Genética , Estudo de Associação Genômica Ampla , Humanos , Polimorfismo Genético , Receptor 5-HT2A de Serotonina/genética , Estudos em Gêmeos como Assunto
19.
Behav Genet ; 42(4): 603-13, 2012 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-22302528

RESUMO

Bulimic behaviors are frequently associated with alcohol use disorders. However, extant family and twin study findings have been inconsistent with regard to whether these behaviors share etiologic influences. A sample of 292 young adult, female twins was used to examine genetic and environmental factors underlying the association between binge eating and compensatory behaviors (e.g., vomiting)and alcohol use. Binge eating and compensatory behaviors were assessed using the Minnesota Eating Behavior Survey.Alcohol use was measured using the Alcohol Use Disorders Identification Test. Univariate models indicated that the heritability of binge eating, compensatory behaviors, and alcohol use was 41, 28, and 78%, respectively, with the remaining variance due to nonshared environmental effects.Bivariate models indicated that there was a moderate-to-large degree of overlap (genetic correlation = 0.31­0.61) in additive genetic factors between alcohol use and binge eating and compensatory behaviors, and no overlap in environmental effects. Findings suggest that these phenotypes co-aggregate in families and that similar genes or heritable traits may be contributing to their co-occurrence.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Alcoolismo/genética , Bulimia/genética , Meio Ambiente , Gêmeos Dizigóticos/genética , Gêmeos Monozigóticos/genética , Adolescente , Adulto , Feminino , Humanos , Modelos Genéticos , Fenótipo , Gêmeos Dizigóticos/psicologia , Gêmeos Monozigóticos/psicologia
20.
Twin Res Hum Genet ; 15(4): 473-82, 2012 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-22854069

RESUMO

BACKGROUND: Previous studies examined caffeine use and caffeine dependence and risk for the symptoms, or diagnosis, of psychiatric disorders. The current study aimed to determine if generalized anxiety disorder (GAD), panic disorder, phobias, major depressive disorder (MDD), anorexia nervosa (AN), or bulimia nervosa (BN) shared common genetic or environmental factors with caffeine use, caffeine tolerance, or caffeine withdrawal. METHOD: Using 2,270 women from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders, bivariate Cholesky decomposition models were used to determine if any of the psychiatric disorders shared genetic or environmental factors with caffeine use phenotypes. RESULTS: GAD, phobias, and MDD shared genetic factors with caffeine use, with genetic correlations estimated to be 0.48, 0.25, and 0.38, respectively. Removal of the shared genetic and environmental parameter for phobias and caffeine use resulted in a significantly worse fitting model. MDD shared unique environmental factors (environmental correlation=0.23) with caffeine tolerance; the genetic correlation between AN and caffeine tolerance and BN and caffeine tolerance were 0.64 and 0.49, respectively. Removal of the genetic and environmental correlation parameters resulted in significantly worse fitting models for GAD, phobias, MDD, AN, and BN, which suggested that there was significant shared liability between each of these phenotypes and caffeine tolerance. GAD had modest genetic correlations with caffeine tolerance, 0.24, and caffeine withdrawal, 0.35. CONCLUSIONS: There was suggestive evidence of shared genetic and environmental liability between psychiatric disorders and caffeine phenotypes. This might inform us about the etiology of the comorbidity between these phenotypes.


Assuntos
Anorexia Nervosa/induzido quimicamente , Transtornos de Ansiedade/induzido quimicamente , Bulimia/induzido quimicamente , Cafeína/efeitos adversos , Transtorno Depressivo Maior/induzido quimicamente , Doenças em Gêmeos/induzido quimicamente , Transtorno de Pânico/induzido quimicamente , Transtornos Fóbicos/induzido quimicamente , Síndrome de Abstinência a Substâncias/genética , Transtornos Relacionados ao Uso de Substâncias/genética , Adulto , Anorexia Nervosa/genética , Anorexia Nervosa/psicologia , Transtornos de Ansiedade/genética , Transtornos de Ansiedade/psicologia , Bulimia/genética , Bulimia/psicologia , Transtorno Depressivo Maior/genética , Transtorno Depressivo Maior/psicologia , Doenças em Gêmeos/genética , Doenças em Gêmeos/psicologia , Feminino , Interação Gene-Ambiente , Humanos , Transtorno de Pânico/genética , Transtorno de Pânico/psicologia , Fenótipo , Transtornos Fóbicos/genética , Transtornos Fóbicos/psicologia , Sistema de Registros , Fatores de Risco , Síndrome de Abstinência a Substâncias/psicologia , Transtornos Relacionados ao Uso de Substâncias/psicologia , Virginia
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