Eating disorders affect 13% of females and contribute to functional impairment and mortality, but few studies have identified risk factors that prospectively correlate with future onset of anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), and purging disorder (PD). Identifying risk factors specific to each eating disorder is critical for advancing etiologic knowledge and designing effective prevention programs.
This study examined whether weight suppression (the difference between a person’s highest past weight at their adult height and their current weight) correlates with future onset of AN, BN, BED, and PD.
Data from 1165 young women with body image concerns (mean ± SD age: 21.9 ± 6.4 y) who completed annual diagnostic interviews over a 3-y follow-up period were examined. Logistic regression models evaluated the relation of baseline weight suppression to onset risk of each eating disorder controlling for age, dietary restraint, and intervention condition.
Elevated weight suppression predicted future onset of AN (OR: 1.36; 95% CI: 1.03, 1.80), BN (OR: 1.34; 95% CI: 1.11, 1.62), PD (OR: 1.46; 95% CI: 1.23, 1.74), and any eating disorder (OR: 1.32; 95% CI: 1.12, 1.56), but not BED (OR: 1.10; 95% CI: 0.89, 1.37). Highest past weight correlated with future onset of BN and PD but not onset of AN, BED, or any eating disorder, and baseline current weight was inversely related to future AN onset only, implying that women with the largest difference between their highest past weight and current weight are at greatest risk of eating disorders.
The results provide novel evidence that weight suppression correlates with future onset of eating disorders characterized by dietary restriction or compensatory weight control behaviors and suggest weight-suppressed women constitute an important risk group to target with selective prevention programs.These trials were registered at clinicaltrials.gov as NCT01126918 and NCT01949649.

Copyright © The Author(s) on behalf of the American Society for Nutrition 2020.

References

PubMed