Exploring differences in disordered eating and related appetitive traits among women based on childhood and current food security status.

Despite emerging evidence that food insecurity (FI) is associated with elevated rates of eating pathology, little is known about the lasting impact of FI on eating behaviors. Studies that have explored the association between FI during childhood and eating behavior in adulthood have not accounted for current FI. The present study explored differences in disordered eating (DE) and related appetitive traits among four groups of cisgender female mothers: individuals who (1) endorsed childhood FI only (n = 96), (2) endorsed current FI only (n = 134), (3) endorsed both childhood and current FI (n = 257), and (4) denied both childhood and current FI (n = 146). Participants responded to online questionnaires including items from the USDA Household Food Security Survey Module, the 7-item Eating Disorder Examination-Questionnaire, the Eating Disorder Diagnostic Scale, and the Adult Eating Behavior Questionnaire. Adjusting for age and race/ethnicity, ANCOVAs explored mean differences between groups in DE and appetitive traits, and a modified Poisson regression model examined differences in binge-eating prevalence across the four FI groups. The "current FI only" group consistently endorsed the highest levels of DE and related appetitive traits followed by the "current and childhood FI" group, suggesting newly food-insecure women may be at highest risk for DE. Interestingly, across almost all constructs, the "childhood FI only" group did not differ significantly from the "no FI" group. These findings suggest that improved access to food may help offset risk for adult DE related to experiences of FI in childhood.

Exploring the possibility of parents' broad internalizing phenotype acting through passive gene-environment correlations on daughters' disordered eating.

Twin studies demonstrate significant environmental influences and a lack of genetic effects on disordered eating before puberty in girls. However, genetic factors could act indirectly through passive gene-environment correlations (rGE; correlations between parents' genes and an environment shaped by those genes) that inflate environmental (but not genetic) estimates. The only study to explore passive rGE did not find significant effects, but the full range of parental phenotypes (e.g., internalizing symptoms) that could impact daughters' disordered eating was not examined. We addressed this gap by exploring whether parents' internalizing symptoms (e.g., anxiety, depressive symptoms) contribute to daughters' eating pathology through passive rGE. Participants were female twin pairs (aged 8-14 years; M = 10.44) in pre-early puberty and their biological parents (n = 279 families) from the Michigan State University Twin Registry. Nuclear twin family models explored passive rGE for parents' internalizing traits/symptoms and twins' overall eating disorder symptoms. No evidence for passive rGE was found. Instead, environmental factors that create similarities between co-twins (but not with their parents) and unique environmental factors were important. In pre-early puberty, genetic factors do not influence daughters' disordered eating, even indirectly through passive rGE. Future research should explore sibling-specific and unique environmental factors during this critical developmental period.