Puberty and the manifestations of loss of control eating in children and adolescents.

Loss of control (LOC) eating refers to the subjective experience of being unable to control what or how much is eaten, regardless of the amount reportedly consumed (1). LOC eating has been well phenotyped, as LOC meals typically are low in protein, high in carbohydrate, and are comprised of highly palatable, energy dense foods (2–4). Pediatric LOC eating is a precursor to partial- and full-syndrome binge eating disorder (BED) and is predictive of exacerbated general and eating disorder psychopathology (5, 6), excessive weight and fat gain (7, 8), and metabolic dysfunction (9). At least one recent episode of LOC eating is reported by 5% to 50% of youth, with higher estimates among adolescent (vs. child), female (vs. male), and overweight (vs. non-overweight) samples (1). LOC eating typically emerges during middle childhood (10) or early adolescence (11, 12). While the presence of a lifetime history of LOC eating has been associated with adverse outcomes (6, 13), only about 50% of youth with LOC eating go on to experience persistent and exacerbated LOC eating patterns during middle to late adolescence and beyond (5, 6, 14). To improve the identification of high-risk youth with LOC eating and refine intervention targets, research is needed to elucidate developmental factors that may contribute to exacerbated disordered eating. Puberty has been identified as a critical risk period for the development of eating disorders and their symptoms, including binge and LOC eating (15). Research on puberty and binge eating lags behind the wealth of data examining the relationship between puberty and other forms of eating disorder psychopathology (15). Pubertal onset, as identified by self-reports of secondary sex characteristics, has been associated with concurrent binge eating among preadolescent girls and boys assessed in the fifth through seventh grades (16, 17). When examining this preadolescent cohort of boys and girls over time, pubertal onset predicted subsequent increases in binge eating frequency (17). Binge eating prevalence was higher at more advanced stages of pubertal development among girls, but not boys, in a large population-based sample, even after accounting for age (18). However, other cross-sectional studies failed to find a significant association between pubertal status and binge eating in girls and boys (19–21). Prior studies’ reliance upon self-report questionnaires to determine both pubertal stage and binge eating severity may have limited reliability and validity relative to interview methods, physical examination, and food intake assessed via laboratory test meals. Moreover, we know of no prior human studies investigating the relationship between pubertal stage and LOC eating. Existing developmental risk models suggest that pubertal development may increase risk for LOC eating through direct and indirect pathways that involve biological and psychosocial factors. Traditional theories posit that the physical changes associated with puberty lead to body dissatisfaction and negative mood, which in turn promote disordered eating behaviors such as classic binge episodes or LOC eating (22, 23). It is hypothesized that girls may be at greater risk for these psychosocial disturbances, as puberty-induced increases in adiposity move girls away from the socially reinforced “thin” body size ideals whereas gains in muscle mass propel boys closer to masculine body ideals (22, 23). Recent theories, by contrast, focus on biological factors and suggest that increases in gonadal hormone levels during puberty play a central role in activating and/or organizing genetic and phenotypic effects that exacerbate disordered eating risk (15). It is also conceivable that pubertal shifts in metabolic hormone levels, which dually regulate eating behaviors and the hypothalamic-pituitary-gonadal axis, may directly promote LOC eating and/or the phenotypic manifestation of LOC eating (24, 25). To date, no known studies have examined the interplay among puberty, LOC eating, and theoretically-driven LOC correlates such as disordered eating attitudes and eating behavior. The current study sought to investigate the association between pubertal development and manifestations of LOC eating in a community sample of children and adolescents. We hypothesized that youth in early-to-mid- and late-pubertal stages would exhibit higher rates of LOC eating than youth in pre-puberty. Based on the mechanisms put forth by psychosocial developmental risk models (22, 23), we hypothesized that associations between LOC eating and concerns about weight and shape would be more robust among post-pubertal youth relative to pre-pubertal youth. Given hypotheses made by biologically-driven developmental risk theories (15), we also expected post-pubertal youth with LOC eating to have greater palatable food consumption in the laboratory, even after adjusting for age and adiposity, relative to pre-pubertal youth with LOC eating and all youth without LOC eating.