Physiological Reactivity, Leptin and Loss of Control Eating in Youth

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DESCRIPTION (provided by applicant): While full-syndrome binge eating disorder (BED) is rarely observed in childhood, loss of control (LOC) eating episodes are often reported by youth.10,11 LOC eating is characterized by eating episodes wherein youth report an experience of lacking of control while eating, irrespective of the amount of food reportedly consumed. Compared with children who do not report LOC eating behaviors, those with LOC are more likely to have greater adiposity, to report increased symptoms of depression and anxiety, disturbed eating cognitions, and lower self-esteem.12 Further, LOC eating in youth may predict the development of partial or full-syndrome BED,13 excess weight gain,14-16 and components of the metabolic syndrome,17 placing them at risk for developing more severe health complications of the cardiovascular and endocrine systems in later life. Among adults with BED, data indicate greater physiological response to stress, including decreased heart rate variability (HRV)18 following laboratory stressors. However, no study has examined physiological responses to laboratory stressors among youth with LOC eating. Additionally, a developing body of research indicates links between HRV, chronic sympathetic activation, and the appetitive hormone leptin, especially among women.19- 27 However, there are limited data examining these relationships in youth.28 To date, no studies have explored the links between LOC eating, laboratory stress, and physiological reactivity in youth. The present study seeks to explore these relationships among overweight girls (8-17 y) with and without LOC eating, using well- validated psychophysiological techniques; specifically salivary cortisol, HRV and serum leptin. We hypothesize that compared to overweight girls without LOC eating, those with LOC eating will have an impaired ability to respond physiologically to laboratory-induced stress, as indicated by decreased cortisol and HRV. We further anticipate that higher leptin levels will be associated with poorer HRV reactivity to a laboratory stressor among youth with LOC eating. Specific aims of the current study are as follows: 1. To explore changes in cortisol and HRV among overweight girls with and without LOC eating following a laboratory stressor; 2. to examine the relationship between baseline plasma leptin and HRV; and 3. to examine the relationship between LOC eating, plasma leptin and HRV. Participants will be 60 overweight girls (8-17y), half of whom will report episodes of LOC eating in the month prior to assessment. Fasting plasma leptin will be collected prior to administration of a laboratory cognitive stressor. Measures of cortisol and HRV will be collected continuously prior to, during, and following the stressor. Subjective measures of perceived stress will be collected at each time point as well. Given that LOC eating may be predictive of a host of adverse psychological and physiological outcomes, the study results will elucidate the nature of LOC eating in youth and its physiological correlates, which will help to inform prevention and intervention efforts for a significant subset of the obese population in an effort t reduce the exacerbation of eating pathology and development of BED.