Abstract
Objectives: To examine the relationship between psychological and social factors (depression, emotional control, sexual abuse, and parental physical punishment) and adolescent drive for Thinness and Bulimic behaviors in a large community sample, and to investigate possible genetic moderation.Method: Data were drawn from the Australian Temperament Project (ATP), a population-based cohort study that has followed a representative sample of 2443 participants from infancy to adulthood across 16 waves since 1983. A subsample of 650 participants (50.2% female) of Caucasian descent who provided DNA were genotyped for a serotonin transporter promoter polymorphism (5-HTTLPR). Adolescent disordered eating attitudes and behaviors were assessed using the Bulimia and Drive for Thinness scales of the Eating Disorder Inventory-2 (15–16 years). Depression and emotional control were examined at the same age using the Short Mood and Feelings Questionnaire, and an ATP-devised measure of emotional control. History of sexual abuse and physical punishment were assessed retrospectively (23–24 years) in a subsample of 467 of those providing DNA.Results: EDI-2 scores were associated with depression, emotional control, and retrospectively reported parental physical punishment. Although there was statistically significant moderation of the relationship between parental physical punishment and bulimic behaviors by 5-HTTLPR (p = 0.0048), genotypes in this subsample were not in Hardy–Weinberg Equilibrium. No other G×E interactions were significant. Conclusion: Findings from this study affirm the central importance of psychosocial processes in disordered eating patterns in adolescence. Evidence of moderation by 5-HTTLPR was not conclusive; however, genetic moderation observed in a subsample not in Hardy–Weinberg Equilibrium warrants further investigation.
Highlights
Eating disorders (EDs) are believed to have a substantial heritable component (Bulik et al, 2016), with estimates from twin studies ranging from 40 to 60% (Yilmaz et al, 2015)
Research examining molecular genetic mechanisms that may increase risk for eating pathology has largely investigated whether certain genetic polymorphisms are found in different frequency in those with a clinical ED compared to controls
Studies examining whether gene by environment (G×E) interactions play a role in ED etiology have largely focussed on 5-HTTLPR, with the short (s) allele associated with lower serotonin transcription activity compared to the long (l) allele (Heils et al, 1996)
Summary
Eating disorders (EDs) are believed to have a substantial heritable component (Bulik et al, 2016), with estimates from twin studies ranging from 40 to 60% (Yilmaz et al, 2015). Research examining molecular genetic mechanisms that may increase risk for eating pathology has largely investigated whether certain genetic polymorphisms (e.g., serotonin transporter linked polymorphism, 5-HTTLPR) are found in different frequency in those with a clinical ED compared to controls. These studies have largely produced inconsistent findings (Calati et al, 2011; Solmi et al, 2016), supporting the notion that genetic risk operates in a manner more complex than simple association. Lack of consensus stems from a range of methodological limitations, such as insufficient sample size, inappropriate statistical techniques and multiple testing, as well as substantial publication bias favoring significant G×E findings (Duncan and Keller, 2011; Duncan et al, 2014; Dick et al, 2015; de Vries et al, 2016)
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