The International journal of eating disorders · 2017
Weight suppression and bulimic syndrome maintenance: Preliminary findings for the mediating role of leptin.
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Keel Pamela K, Bodell Lindsay P, Haedt-Matt Alissa A, Williams Diana L, Appelbaum Jonathan
Аннотация
OBJECTIVE: Longitudinal studies support a prospective relationship between weight suppression (WS) and bulimic syndrome (BN-S) maintenance. Although biobehavioral mechanisms have been proposed to explain this link, such mechanisms have yet to be identified. Given that weight loss would reduce leptin levels which may influence eating, this study examined whether reduced leptin levels mediate the link between greater WS and longer illness duration.
METHOD: Women (N = 53), ages 18-45 years, were recruited from the community if they met criteria for a BN-S, including either DSM-5 bulimia nervosa (BN; n = 33) or purging disorder (PD: n = 20), and fell within a healthy weight range (18.5-26.5 kg/m2 ). Participants completed clinical assessments and provided blood samples to measure circulating leptin.
RESULTS: Significant associations were found among greater WS, lower leptin concentrations, and longer duration of illness. Mediation analyses using bootstrapping procedures indicated all paths were significant and that leptin mediated the link between WS and illness duration. An alternative model in which longer illness duration contributed to leptin, via greater WS, was not supported.
DISCUSSION: Longitudinal research is needed to support temporal associations and explore behavioral mechanisms linking leptin to illness trajectory.
METHOD: Women (N = 53), ages 18-45 years, were recruited from the community if they met criteria for a BN-S, including either DSM-5 bulimia nervosa (BN; n = 33) or purging disorder (PD: n = 20), and fell within a healthy weight range (18.5-26.5 kg/m2 ). Participants completed clinical assessments and provided blood samples to measure circulating leptin.
RESULTS: Significant associations were found among greater WS, lower leptin concentrations, and longer duration of illness. Mediation analyses using bootstrapping procedures indicated all paths were significant and that leptin mediated the link between WS and illness duration. An alternative model in which longer illness duration contributed to leptin, via greater WS, was not supported.
DISCUSSION: Longitudinal research is needed to support temporal associations and explore behavioral mechanisms linking leptin to illness trajectory.