Social Responsiveness and Objectification: The Moderating Roles of Serotonin Transporter and Serotonin Receptor 2A Genotypes in an Objectification Theory Model of Disordered Eating

• Published in: Sex roles 2020-05, Vol.82 (9-10), p.584-599
• Main Authors: Sullivan, Grace A., Gervais, Sarah J., Brock, Rebecca L., Stoltenberg, Scott F.
• Format: Article
• Language: English
• Subjects: Behavioral Science and Psychology; Eating disorders; Females; Feminism; Gender Studies; Genetics; Human body; Medicine/Public Health; Original Article; Psychology; Resistance (Psychology); Serotonin; Shame; Sociology; Surveillance; Women
• ISSN: 0360-0025; 1573-2762
• DOI: 10.1007/s11199-019-01075-3

Feminist scholars have called for gender researchers to consider gene-environment interactions for gender-imbalanced disorders (Salk and Hyde Psychology of Women Quarterly, 36 , 395–411, 2012 ). Responding to these calls, the present study integrates objectification theory (Fredrickson and Roberts Psychology of Women Quarterly, 21 , 173–206, 1997 ) and genetic research. In the tested model, objectification experiences are associated with disordered eating through body surveillance and body shame, and serotonin transporter ( SLC6A4 ) genotypes (5-HTTLPR and rs25531), serotonin 2A receptor SNP genotypes (HTR2A rs6311), and the epistatic interaction between those genotypes function as moderators. U.S. undergraduate women ( n  = 526) completed self-reports of objectification, body surveillance, body shame, and disordered eating and donated buccal cells for genetic analyses. The association between objectification and disordered eating was mediated by body shame, but not body surveillance. The paths from objectification to both body surveillance and body shame were moderated by genotypes. The indirect effect of objectification on disordered eating through body shame was only present for SLC6A4 L′ and rs6311 G homozygotes. Our results are consistent with previous evidence that serotonin system genetic variation is associated with disordered eating risk. They provide evidence of a non-deterministic genetic effect that is context-dependent and subtle. These findings also reinforce efforts to develop personalized prevention and treatment approaches for eating disorders.