Binge Eating and Metabolic Dysfunction, 1 Running Head: BINGE EATING AND METABOLIC DYSFUNCTION IN YOUTH Binge Eating, Urine-Free Cortisol, and Metabolic Characteristics in Children and Adolescents

Overweight youth are likely to exhibit disordered eating pathology, specifically binge eating behaviors. Preliminary research indicates that binge eating and associated psychopathology in youth are associated with components of the metabolic syndrome. While metabolic dysfunction is inherently tied to obesity, some preliminary studies have found that binge eating and psychological stress are independently associated with metabolic dysfunction. This study explored the relationship between binge eating and metabolic dysfunction, and the potential mediating role of cortisol among children and adolescents. Participants were 396 overweight and non-overweight youth between the ages of 5 and 18 years. Children with binge eating had significantly greater total cholesterol, LDL cholesterol, waist circumference, insulin resistance and insulin levels than children without binge eating (ps ≤.05). However, BMI-z (standard deviations of BMI based on CDC growth charts) accounted for most of the results. There were no significant differences in HDL, blood pressure, and triglyceride levels among individuals with out without binge eating (ps >.05). Among adolescents, relationships existed between urine free cortisol and LDL cholesterol, even after adjusting for BMI-z, age, sex, and race (ps ≤ .05). Binge eating was unrelated to cortisol. We conclude that binge eating in youth may be related to metabolic dysfunction, but these associations are primarily accounted for by the links that binge eating has with body weight. Given the prevalence of binge eating among children, longitudinal research is warranted to examine whether children’s binge eating exerts a unique effect on metabolic characteristics beyond its effects on weight gain. Binge Eating and Metabolic Dysfunction, 3 Background and Significance The Problem: Obesity in Youth. Obesity is a growing national concern. Rates have risen dramatically among children and adolescents over the past 30 years (Ogden, Carroll, Curtin, Lamb, & Flegal, 2010). According to recent estimates, between 2007 and 2008, approximately 13% of children and adolescents, aged 6 to 19 years old, are overweight (body mass index, BMI, kg/m, ≥ 97 percentile for age and sex) (Ogden et al., 2010). Overweight in childhood and adolescence (BMI between the 85 and 95 percentile) is a risk factor for obesity in adulthood (Field, Cook, & Gillman, 2005). Furthermore, individuals who are obese (BMI > 95 percentile) are at greater risk than their non-obese counterparts for a variety of negative health consequences including heart disease, respiratory problems, hormonal dysfunction, osteoarthritis, certain cancers, and liver disease (Bray, 2003). Childhood obesity is associated with health problems in adulthood (Dietz, 1998). Additionally, obesity during childhood or adolescence places an individual at risk for developing health problems during youth (e.g., hypertension, hyperlipidemia, and insulin resistance) (Dietz, 1998). Physiological Outcomes of Obesity in Children: Metabolic Syndrome. One particularly severe, and well established association with obesity in adulthood is metabolic syndrome (Zimmet et al., 2007). The metabolic syndrome (also known as syndrome X) is characterized by the following cluster of markerss: insulin resistance, central obesity, higher than normal triglyceride levels, lower than normal levels of HDL cholesterol, dyslipidemia and hypertension. In combination, these physiological markers dramatically increase an individual’s risk for developing heart disease and risk for type 2 diabetes (up to 30 times more than the rest of the population). The more physiological markers present, the greater the risk for heart disease and diabetes. Central, abdominal obesity (as opposed to peripheral obesity, or excess fat in the Binge Eating and Metabolic Dysfunction, 4 hips, thighs, and buttocks) has a strong relationship with cardiovascular disease. This type of obesity is perhaps the greatest risk factor for metabolic syndrome, and is characterized by increased production of cortisol (Bjorntorp & Rosmond, 2000a). Currently, there exist three widely used definitions of metabolic syndrome in adults, from the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP III), the World Health Organization (WHO) and the International Diabetes Federation (IDF). The common features of these three definitions are that all use the same five criterion components and require a minimum of three symptoms to meet diagnostic criteria. However, the specific cut-offs to qualify as “symptomatic” vary (Huang, Ball, & Franks, 2007). Additionally, the WHO definition requires a diagnosis of either diabetes, impaired fasting glucose, impaired glucose tolerance or insulin resistance for a metabolic syndrome diagnosis. The IDF definition requires the presence of central obesity. A major problem with the WHO definition is that it does not identify those merely at risk for diabetes, but rather those with a full disorder, which may be problematic in studies of younger populations (Huang et al., 2007). Researchers and clinicians have not yet reached a consensus on a universal definition for metabolic syndrome in children. In particular, there are discrepancies in terms of which components of metabolic syndrome should be considered risk factors for heart disease and diabetes (e.g., abdominal obesity, triglycerides). Additionally, there is variation in the cut-offs used for each component of the metabolic syndrome to be considered “at risk” for heart disease or diabetes (Huang et al., 2007). As a result, many studies have adapted adult definitions of metabolic syndrome to apply to pediatric populations, which translates into a great deal of variability in cut-offs for certain risk factors among younger populations. Despite a lack of a clear definition, the estimated prevalence of metabolic syndrome in children seems to mirror Binge Eating and Metabolic Dysfunction, 5 rates of obesity and overweight in youth worldwide, indicating a strong relationship between these two variables ((Invitti et al., 2006). Rates vary widely, from 0-26% of metabolic syndrome present in preadolescent girls, depending on the definitions and cut-offs used (Chi, Wang, Wilson, & Robinson, 2006). Among adolescent boys and girls (between 12 and 19 years of age) from NHANES III data collected between 1988 and 1994 (de Ferranti et al., 2004), full metabolic syndrome was prevalent among 9.2% of the sample (9.5% of boys vs. 8.9% of girls). However, among this sample, 63.4% had at least one metabolic abnormality in one of the above five components (de Ferranti et al., 2004). Metabolic syndrome is most prevalent among overweight youth (28.7% of overweight adolescents aged 12-19 in the U.S.) compared to a prevalence of 0-1% among normal weight youth (Chi et al., 2006). Additionally, Weiss et al. (2004) estimated that as many as 50% of severely obese children had a metabolic syndrome. Youth particularly at risk for metabolic dysfunctions include African-American, Hispanic, South Asian, Native American, Pacific Islander, and First Nation Canadian (Huang et al., 2007). Screening for Metabolic Syndrome. Components of the metabolic syndrome tend to cluster, and in combination, exponentially increase risk for cardiovascular disease and type II diabetes. The Bogalusa Heart Study (Chen, Srinivasan, Elkasabany, & Berenson, 1999) identified two specific clusters of syndromes in youth, the first combining fasting insulin, HDL, and triglycerides. The second cluster was composed of fasting insulin and blood pressure. These two clusters were found to be highly heritable, and symptoms tended to manifest early on in childhood and remain stable into adulthood (Eisenmann, Welk, Wickel, & Blair, 2004). While there is a lack of consensus in terms of what constitutes metabolic syndrome in youth, Huang et al. (2007) highlight the importance of screening for any of the five symptoms of the disorder, as each individually can be a risk for severe outcomes in child and adulthood. The Binge Eating and Metabolic Dysfunction, 6 presence of one or more symptoms (rather than the standard three in adults) may be vital for identifying youth who are at greatest risk for disease and who can benefit from early intervention. Additionally, while no pre-determined, meaningful cut-offs currently exist for each component, many researchers continue to use adult criteria, which may be problematic, as the levels of metabolic dysfunction may present differently in children and adolescents. Risk Factors of Metabolic Syndrome in Youth. Obesity is considered a primary cause of insulin resistance and metabolic syndrome in youth, and it, in turn, may be caused by a variety of factors including genetic, endocrine, psychiatric and socioeconomic. It is thought that the prevention or treatment of obesity in youth can offset the negative trajectory of metabolic syndrome (Biltoft & Muir, 2009). There is relatively weak support for a link between physical inactivity and metabolic syndrome in youth, with only one study indicating a positive association between physical inactivity and increased insulin levels, triglycerides and adiposity, indicating that other factors may be operating in the development of metabolic syndrome (Craig, Bandini, Lichtenstein, Schaefer, & Dietz, 1996). Overall quality of diet does seem to predict metabolic dysfunction; however, this relationship is poorly understood. In general, increases in carbohydrate and decreases in fat consumption are positively associated with insulin sensitivity, and increases in fat intake are associated with lower insulin sensitivity, and fruit and vegetable intake may protect against several components of the metabolic syndrome (Huang et al., 2007). Components of the Metabolic Syndrome. Among adults and children, it is thought that central obesity and insulin resistance are the best predictors of metabolic syndrome, and drive all other components of the syndrome