Genetic factors account for over 70% of the variance in fussy eating behaviors from toddlerhood to early adolescence, according to a recent study.
Using data from the Gemini twin cohort, a population-based sample of 4,804 British twins born in 2007, researchers assessed food fussiness from ages 16 months to 13 years with the Child Eating Behaviour Questionnaire. Parents provided reports on fussy eating when the children were 16 months (n = 3,854), 3 years (n = 2,666), 5 years (n = 2,098), 7 years (n = 703), and 13 years old (n = 970).
A single trajectory of food fussiness was modeled, showing an increase from 16 months to 7 years, followed by a slight decline between 7 and 13 years.
At 16 months, genetic influence on fussy eating was estimated at 60% (95% confidence interval [CI]: 53%-67%) and increased significantly after toddlerhood, reaching 83% (95% CI: 81%-86%) by age 3 and peaking at 84% across all ages. This demonstrated that fussy eating behaviors are highly stable and primarily driven by genetics.
Shared environmental factors accounted for 25% of the variation in food fussiness at 16 months but became negligible by age 3. Unique environmental factors contributed to 15%-26% of the variance in fussy eating across all age points, with lasting effects observed from age 5 onward.
The shared environment had a notable effect during toddlerhood but diminished as children aged, while unique environmental factors, though contributing a smaller portion of the variance compared to genetics, persisted throughout development. Significant correlations were observed between genetic and unique environmental factors across different components of fussy eating.
Positive correlations between the intercept and linear slope indicated that the same genetic and unique environmental influences contributing to higher fussy eating scores in toddlerhood were also associated with an increase in fussy eating from toddlerhood to middle childhood. Additionally, unique environmental influences grew as children gained more independence over time.
Age trajectory was analyzed using a mixed linear model, while a correlated factors twin model was used to evaluate genetic and environmental contributions to variation. Additionally, a longitudinal ACE Cholesky Decomposition Model was applied to explore these influences at each discrete age across five-time points. For a more streamlined model, the shared environmental (C) paths for ages 3, 5, 7, and 13 were excluded due to their minimal and non-significant influence, without affecting the model’s fit. However, the C path was retained for 16 months as its contribution was both substantial and statistically significant.
The study, published in The Journal of Child Psychology and Psychiatry, suggests that early interventions may be effective during periods when environmental factors are more influential, particularly in toddlerhood. Given the strong genetic component, interventions may need to be tailored to individual genetic profiles as children develop.
The authors have declared no conflicts of interest.