Food fussiness and food neophobia share a common etiology in early childhood. (14th October 2016)

• Record Type: Journal Article
• Authors: Smith, Andrea D.; Herle, Moritz; Fildes, Alison; Cooke, Lucy; Steinsbekk, Silje; Llewellyn, Clare H.
• Is Part Of: Journal of child psychology and psychiatry and allied disciplines. Volume 58:Number 2(2017)
• Page Start: 189
• Page End: 196
• Publication Date: 2016-10-14
• Subjects: Eating behavior -- twin design -- behavioral genetics -- food fussiness -- food neophobia; Child psychology -- Periodicals; Child psychiatry -- Periodicals; 155.4
• DOI: 10.1111/jcpp.12647
• Languages: English
• ISSNs: 0021-9630

Abstract

Abstract : Background: 'Food fussiness' (FF) is the tendency to be highly selective about which foods one is willing to eat, and emerges in early childhood; 'food neophobia' (FN) is a closely related characteristic but specifically refers to rejection of unfamiliar food. These behaviors are associated, but the extent to which their etiological architecture overlaps is unknown. The objective of this study was to quantify the relative contribution of genetic and environmental influences to variation in FF and FN in early childhood; and to establish the extent to which they share common genetic and environmental influences. Method: Participants were 1, 921 families with 16‐month‐old twins from the Gemini birth cohort. Parents completed the Child Eating Behaviour Questionnaire which included three FF items and four FN items. Bivariate quantitative genetic modeling was used to quantify: (a) genetic and environmental contributions to variation in FF and FN; and (b) the extent to which genetic or environmental influences on FF and FN are shared across the traits. Results: Food fussiness and FN were strongly correlated ( r = .72, p < .001). Proportions of variation in FF were equally explained by genetic (.46; 95% CI: 0.41–0.52) and shared environmental influences (.46; 95% CI: 0.41–0.51). Shared environmental effects accounted for a significantly lower proportion of variation in FN (.22; 95% CI: 0.14–0.30), but genetic influences were not significantly different from those on FF (.58, 95% CI: 0.50–0.67). FF and FN largely shared a common etiology, indicated by high genetic (.73; 95% CI: 0.67–0.78) and shared environmental correlations (.78; 95% CI: 0.69–0.86) across the two traits. Conclusions: Food fussiness and FN both show considerable heritability at 16 months but shared environmental factors, for example the home environment, influenced more interindividual differences in the expression of FF than in FN. FF and FN largely share a common etiology.