Adolescent disordered eating and epigenetic age acceleration.

Disordered eating encompasses both clinical eating disorders, and disordered eating-related behaviours and cognitions that may not meet full diagnostic criteria for an eating disorder, but still cause significant distress. Studies have shown that disordered eating behaviours such as dietary restriction, excessive exercise, binge eating, and purging, often result in severe health issues affecting multiple organ systems, including immune, metabolic, and stress-related processes [–]. Further, the cognitions that accompany disordered eating behaviours, such as distorted thoughts about body weight or the need to control food intake, often cause increased psychological stress [], leading to the activation of physiological stress responses including increased inflammation, lowered immune response, and impaired psychosocial functioning []. Biological ageing, referring to the progressive decline of physiological function, tissue structure, and organ integrity over time, may be a pathway through which disordered eating influences these health outcomes []. Biological ageing can be defined through multiple biological systems and has been measured using clinical biomarkers, such as white blood cell count and C-reactive protein [, ], and also epigenetic variation (epigenetic age) through the use of epigenetic clocks which measure changes in DNA methylation patterns [, –]. DNA methylation involves the addition of a methyl group to a cytosine base at a CpG site and can result in affected genes being suppressed or silenced [, ]. DNA methylation has been investigated in those with eating disorders, however most studies have focused on anorexia nervosa (AN) [], with a smaller number investigating bulimia nervosa and binge eating disorder [–]. No studies have investigated DNA methylation in people with disordered eating more broadly. DNA methylation studies on eating disorders using candidate gene and global methylation approaches have been mixed and yielded inconsistent findings []. More recently, epigenome-wide association studies (EWAS) have identified differentially methylated CpG sites associated with eating disorders (primarily AN) in genes related to metabolic, psychological, and immune functioning [, –]. Studies have consistently demonstrated increased DNA methylation among individuals with AN [–], and chronicity of AN has been associated with variations in DNA methylation in regions linked to genes associated with immunity, anxiety, metabolism, serotonin, insulin, and central nervous system function [, , ].