Findings with 0.25 mg dexamethasone suppression test in eating disorders: Association with childhood trauma
Department of Psychiatry, Hospital Clínico San Carlos, Madrid, Spain. CNS spectrums
(Impact Factor: 2.71).
While both blunted and enhanced cortisol suppression following a dexamethasone suppression test (DST) are described in eating disorders, some evidence suggests that enhanced cortisol suppression might be associated with the presence of trauma history. The objective of this study is to investigate hypothalamic-pituitary-adrenal axis response to a modified DST in eating disorders and its relationship with childhood trauma.
Fifty-two patients with eating disorders were studied with a 0.25 mg DST and with measures of childhood trauma.
Patients with bulimia symptoms had significantly greater cortisol suppression than controls and restrictive anorexia patients (F=8.2, P<.05). Cortisol suppression was significantly correlated with intensity of childhood traumatic events (F=0.32, P<.05). Hypersensitive hypothalamic-pituitary-adrenal axis response to DST in eating disorders may be related with a history of childhood trauma and suggests some biological similarities with posttraumatic syndromes that should be further explored.
Available from: Marian Tanofsky-Kraff
- "These disturbances are linked to abnormal NVS responses often observed among individuals with binge-type EDs and psychological risk factors for LOC eating. Such stressor-induced biological alterations may serve as mechanisms through which sustained childhood stressors increase risk for binge-type EDs (Steiger et al. 2001; Díaz-Marsá et al. 2007). Childhood appears to represent a sensitive period for the impact of chronic stressors, as more persistent and atypical neurodevelopmental alterations in corticolimbic circuitry emerge when sustained threats and losses occur at an earlier age and for a longer duration (Lupien et al. 2009). "
[Show abstract] [Hide abstract]
ABSTRACT: Pediatric loss-of-control (LOC) eating is a robust behavioral precursor to binge-type eating disorders. Elucidating precursors to LOC eating and binge-type eating disorders may refine developmental risk models of eating disorders and inform interventions.
We review evidence within constructs of the Negative Valence Systems (NVS) domain, as specified by the Research Domain Criteria framework. Based on published studies, we propose an integrated NVS model of binge-type eating-disorder risk.
Data implicate altered corticolimbic functioning, neuroendocrine dysregulation, and self-reported negative affect as possible risk factors. However, neuroimaging and physiological data in children and adolescents are sparse, and most prospective studies are limited to self-report measures.
We discuss a broad NVS framework for conceptualizing early risk for binge-type eating disorders. Future neural and behavioral research on the developmental trajectory of LOC and binge-type eating disorders is required.
Available from: Xuefeng Gu
[Show abstract] [Hide abstract]
ABSTRACT: To examine the neurobiological basis of bingeing-related eating disorders using an animal model system.
Sprague-Dawley pups were separated from dam for 3 h daily during the first two weeks of birth (maternal separation (MS)), or left undisturbed (non-handled (NH)). Pups were subjected to repeated fasting/refeeding (RF) cycles; that is, 24 h food deprivation and 24 h RF (NH/RF or MS/RF), or had free access to food and water (NH/fed control (FC) or MS/FC) from postnatal day (PND) 28-40.
Body weight gain and food intake were recorded. The arcuate expression of neuropeptide Y (NPY) and plasma corticosterone levels were analyzed on PND 29 and 40.
Decrease in weight gain by repeated fasting/RF cycles was smaller in MS pups than in NH. Interestingly, weight changes responding to fasting or RF increased in MS/RF compared with NH/RF. Compensatory hyperphagia was diminished in NH/RF after the third fasting trial, but persisted in MS/RF throughout the experimental period. The arcuate expression of NPY mRNA responding to food deprivation was blunted, but elevation of plasma corticosterone exaggerated, in the MS group, compared to the NH group, on PND 29 after the first fasting session. However, both the arcuate NPY mRNA and plasma corticosterone levels were increased in MS/RF, but not in NH/RF, on PND 40 after the six sets of fasting/RF cycles, compared to the free FC groups.
Experience of neonatal MS may lead to an exaggerated feeding response to repeated fasting/RF challenges at adolescence, perhaps, due to increased responsiveness of the hypothalamic-pituitary-adrenal gland axis. Additionally, the results suggested that an increased action of the hypothalamic NPY may not be necessary to induce compensatory hyperphagia following food deprivation.
Available from: Katherine E Wynne-Edwards
[Show abstract] [Hide abstract]
ABSTRACT: There is widespread consensus that stress induces dramatic physiological changes, but no agreement on the quantitative parameters that are appropriate to measure these responses. More importantly, the interpretation of various stress measurements, and how individual responses should be evaluated, has not been properly addressed. Even the definition of baseline, against which stress responses must be measured, is not clearly established. The current experiment sought to address these shortcomings by comparing the predictive value of different calculated parameters for psychosocial and physiological measures of stress across individuals. Subjects were 29 male and 59 female healthy undergraduate students with saliva samples collected over a 3-h interval that included a Trier Social Stress Test. Salivary cortisol and alpha-amylase response were analyzed using the absolute concentration, the percent change in concentration, the area under the curve (Pruessner et al., 2003), and the arrival index (change from arrival to 1h after arrival). The arrival index correlated with the subsequent stress response for both cortisol (r=0.76, p<0.01) and alpha-amylase (r=0.86, p<0.01). The arrival index for both cortisol and alpha-amylase was also related to subjective ratings of anxiety following the psychosocial stressor. A subset of individuals with high self-reported anxiety also displayed higher reactivity in response to the psychosocial stressor. Thus, the magnitude of the difference in cortisol and alpha-amylase between arrival and 1h after arrival was a predictor of subsequent stress reactivity. These findings suggest that different psychosocial profiles may be reflected in cortisol and alpha-amylase changes. For this reason: (1) a recovery period after arrival is essential to establish a baseline, (2) the difference between arrival and post-recovery period baseline should be included in experimental designs as a predictive variable, and (3) transformation of individual measures into proportional changes relative to the arrival sample is very likely to obscure important underlying individual differences.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.