Does binge eating disorder alter cortisol secretion in obese women?

Obesity and Eating Disorders Group (GOTA) - Instituto Estadual de Diabetes e Endocrinologia (IEDE)/Instituto de Psiquiatria da Universidade Federal do Rio de Janeiro (IPUB/UFRJ), Rio de Janeiro, Brazil.
Eating Behaviors (Impact Factor: 1.58). 02/2007; 8(1):59-64. DOI: 10.1016/j.eatbeh.2006.01.002
Source: PubMed


It is still poorly determined whether the presence of Binge Eating Disorder (BED) would alter cortisol secretion in obese patients. We aimed at investigating levels of salivary cortisol (SC) in patients with and without BED. Forty seven (47) obese women between 30 and 65 years old were sequentially selected to participate in the study. The diagnosis of BED was assessed according to the Structured Clinical Interview for DSM-IV. Binge Eating Scale (BES) was used to assess binge severity. A trend toward a negative correlation was observed between SC and body mass index in the whole sample (p=0.06). The presence of BED was not associated with increased levels of SC. In women without BED, SC levels correlated inversely with BMI (p=0.01). On the other hand, in women with BED, SC levels correlated significantly with BES (p=0.01). Although obesity is associated with decreased levels of cortisol, this relationship may be lost in patients with BED. In patients with BED, binge eating severity may be a more relevant regulator of cortisol secretion than obesity itself.

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    • "Cortisol suppression after dexamethasone administration has been shown to be normal in this population (Yanovski et al., 1993; Gluck et al., 2004). Single measurement evening cortisol (Coutinho et al., 2007), as well as morning cortisol levels, have been reported to be normal both in obese as well as in non-obese women with BED (Monteleone et al., 2000; Monteleone et al., 2003). In contrast, overall cortisol secretion as reflected by repeated cortisol measurements during the day for two consecutive days was found to be significantly lower in obese women with BED in comparison to obese women without BED (Larsen et al., 2009). "
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    ABSTRACT: While stress and negative affect is known to precede "emotional eating", this relationship is not fully understood. The objective of this study was to explore the relationship between induced psychological stress, HPA axis and eating behavior in Binge Eating Disorder (BED). The Trier Social Stress Test (TSST) was applied in obese participants with (n=8) and without BED (n=8), and normal weight controls (n=8). Psychological and eating-related symptoms, and cortisol secretion were assessed. Baseline stress, anxiety and cortisol measures were similar in all groups. At baseline desire to binge was significantly higher among the BED group. While the TSST induced an increase in cortisol levels, a blunted cortisol response was observed in the BED group. In the BED group, a positive correlation was found between cortisol (area under the curve) levels during the TSST and the change in VAS scores for desire to binge. Post-TSST desire to binge and sweet craving were significantly higher in the BED group and correlated positively with stress, anxiety, and cortisol response in the BED group only. These results suggest chronic down-regulation of the HPA axis in participants with BED, and a relationship between psychological stress, the acute activation of the HPA axis, and food craving.
    10/2012; 208(2). DOI:10.1016/j.psychres.2012.09.050
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    • "Coutinho [27] "
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    ABSTRACT: This chapter focuses on salivary cortisol in relation to biological markers. Specifically, associations with conventional cardiovascular risk factors and metabolic abnormalities (body mass index, waist circumference, waist/hip ratio, lipid status, glucose, blood pressure, heart rate and heart rate variability), markers related to inflammation (C-reactive protein, cytokines and tumor necrosis factor-alpha) and other stress hormones (adrenaline and noradrenaline) were studied. The focus was on healthy adult populations; studies on patient populations and pregnant women were excluded. Studies on genome variations and pharmacological interventions were also excluded. After meeting all exclusion criteria, 42 papers remained. In total, 273 associations between salivary cortisol and any of the markers mentioned were studied, comprising 241 associations on metabolic abnormalities, 30 on inflammation, and 2 on stress hormones. Of the salivary cortisol measures reported for evaluations of all markers tested were 136 (49%) single time points, 100 (37%) deviations, 36 (13%) AUC, and 1 (1%) dexamethasone test. Of these, 72 (26%) were statistically significant, and 201 (74%) indicated non-significant findings.Several of the markers tested showed low or no association with any of the measurements of salivary cortisol. The number of studies exploring the association between cortisol in saliva and markers for inflammation is low, which limits the possibility of interpretation. The number of studies on adrenaline and noradrenaline is also low. To sum up, the proportion of non-significant findings was considerable. This may be due to a large number of studies with relatively small study populations. This is true for metabolic abnormalities, markers related to inflammation as well as other stress hormones. Further studies on inflammatory markers and approaches designed to study variability in other systems in relation to cortisol variability are required.
    01/2012: pages 87-115;
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    ABSTRACT: The etiopathogenesis of eating disorders (ED) is complex and poorly understood. Biological, psychological and environmental factors have all been considered to be involved in the onset and the persistence of these syndromes, often with conflicting results. The recent literature focused on the possible role of hormonal pathways, in particular the hypothalamic-pituitary-adrenal (HPA) axis, as a relevant factor capable of influencing the onset and the course of ED. Other studies have suggested that the onset of ED is often preceded by severe life events, and that chronic stress is associated with the persistence of these disorders. As the biological response to stress is the activation of the HPA axis, the available literature considering the relationships between stress, HPA axis functioning and anorexia nervosa, bulimia nervosa and binge eating disorder is reviewed by the present article.
    Neuropsychobiology 07/2008; 57(3):95-115. DOI:10.1159/000138912 · 2.26 Impact Factor
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