Circadian cortisol profiles, anxiety and depressive symptomatology, and body mass index in a clinical population of obese children

Abstract

Obesity is highly co-morbid with anxiety and/or depression in children, conditions that may further worsen the metabolic and cardiovascular risks for obese individuals. Dysregulation of the hypothalamic-pituitary-adrenal axis is involved in the pathophysiology of anxiety disorders, depression, and obesity, and diverse cortisol concentrations may be found in obese children, depending on their degree of psychological distress. The aim of this study was to examine cortisol profiles among obese children with or without symptoms of anxiety and depression. A group of 128 children (53% females; mean age ± SD: 11.2 ± 2.2 years) derived from a pediatric obesity clinic were studied. Anxiety and depressive symptomatology were assessed with appropriate instruments. Morning serum and five diurnal salivary cortisol concentrations were measured. Obese children were 3.1/2.3 times more likely to report state and trait anxiety, respectively, and 3.6 times more likely to report depressive symptoms than children of the same age group, from a contemporary Greek sample. Trait anxiety and noon salivary cortisol concentrations were significantly positively correlated (p = 0.002). Overall, salivary cortisol concentrations were increased in children with anxiety or depression symptomatology compared to obese children without any affective morbidity (p = 0.02) and to those with anxiety and depression co-morbidity (p = 0.02). In conclusion, in obese children, emotional distress expressed by symptoms of anxiety and/or depression is associated with circadian cortisol profiles reflecting a potential pathway for further morbidity. Longitudinal studies may reveal a role of cortisol in linking obesity, anxiety, and depression to the development of further psychological and physical morbidity.

Obesity and onset of depression among U.S. middle-aged and older adults

“…Dysregulation of the HPA axis is found among obese and depressed subjects and both anti-obesity drugs and antidepressants regulate the HPA axis [36], suggesting potential pathway between obesity and depression through the stress-response system. Pervanidou et al [37] provided preliminary evidence on the stress-response system pathway. They found increased cortisol concentrations among obese children with comorbid depression or anxiety compared with obese children without any affective disorders.…”

Disordered Eating Attitudes and Behaviors in Youth with Overweight and Obesity: Implications for Treatment

“…Rates of disordered eating attitudes and behaviors are higher in children with obesity than in children in the normal-weight range [2]. Childhood obesity and disordered eating attitudes and behaviors are each associated with numerous physical health issues that track into adulthood as well as increased psychological and social problems, including full-syndrome eating disorder (ED) development, such as binge eating disorder (BED) or bulimia nervosa (BN), internalizing symptoms, such as symptoms of depression or anxiety, and peer and family problems, including teasing and potentially harmful parent-child feeding practices [3–10]. Current research suggests that physical health issues and psychosocial problems may be exacerbated in children who experience both obesity and disordered eating attitudes and behaviors, making this group particularly vulnerable [7, 9, 8].…”

Early-Life Stress: From Neuroendocrine Mechanisms to Stress-Related Disorders

“…Disturbed eating behaviors, such as emotional and external eating patterns, are potential mediators of this association [30]. In a previous study, we found an increased prevalence of internalizing and externalizing symptoms in a clinical population of obese children in comparison to normal-weight ones [49], whereas, in a second study, emotional distress expressed by symptoms of anxiety and/or depression in obese children was associated with disturbed diurnal cortisol profiles reflecting a potential pathway for further morbidity [50]. …”