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Parental substance use and child reward-driven eating behaviors.

ABSTRACT: Family history of substance use is a well-established risk factor for greater substance use in adolescence and adulthood. The biological vulnerability hypothesis proposes that family history of substance use might also confer risk for obesogenic eating behavior because of similar rewarding characteristics between substances and certain foods (e.g., processed foods high in refined carbohydrates and fat). Indeed, preliminary research shows that family history of substance use is linked with sweet liking and obesity in adults; however, it is unknown whether this factor is linked to eating behavior earlier in development. The present study (n?=?52) tested the association of severity of parental nicotine dependence and alcohol use (drinking frequency, drinking quantity, binge drinking, and number of annual drinks consumed) with two types of child [M_age?=?10.18 (0.83) years] eating behavior: homeostatic eatingbehavior, or eating regulated by internal satiety cues, and reward-driven eatingbehavior, or eating motivated by pleasure. Results indicated that-over and above the influence of child age, child biological sex, and family income-more severe parental nicotine dependence and frequent and/or heavy, frequent parental alcohol use were associated with significantly greater child reward-driven eating behaviors as indexed by the Food Responsiveness and Enjoyment of Food subscales on the Child Eating Behavior Questionnaire. Parental substance use was not associated with child homeostatic eating behavior as indexed by the Satiety Responsiveness subscale. Family history of substance use may be an important transdiagnostic risk factor that identifies children at risk for obesogenic, reward-driven eating behaviors.

SUBMITTER: Cummings JR

PROVIDER: S-EPMC6890229 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Parental substance use and child reward-driven eating behaviors.

Cummings Jenna R JR Lumeng Julie C JC Miller Alison L AL Hyde Luke W LW Siada Ruby R Gearhardt Ashley N AN

Appetite 20191009

Family history of substance use is a well-established risk factor for greater substance use in adolescence and adulthood. The biological vulnerability hypothesis proposes that family history of substance use might also confer risk for obesogenic eating behavior because of similar rewarding characteristics between substances and certain foods (e.g., processed foods high in refined carbohydrates and fat). Indeed, preliminary research shows that family history of substance use is linked with sweet ...[more]

PMID: 31605723

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Project description:BackgroundStudies have reported that impulsivity predicts childhood BMI and that the association is mediated by eating behaviors. One aspect of impulsivity-potentially crucial in the obesity context-is reward responsiveness, which may predispose to responsiveness to palatable food cues. The behavioral susceptibility theory hypothesizes that genetic susceptibility to obesity operates partly via genetically determined differences in appetite regulation. Reward responsiveness may therefore be one of the neuro-endophenotypes that mediates genetic susceptibility to obesity.ObjectiveTo test whether reward responsiveness, eating behaviors, and child BMI share common genetic architecture.MethodsWe examined reward responsiveness, eating behaviors, and BMI in 5-year-old children from Gemini, a UK birth cohort of 2402 twin pairs born in 2007. All measures were collected by parent report. Reward responsiveness was derived from the Behavioral Approach System. Compulsion to eat and eating for pleasure was measured with the "food responsiveness" scale of the Child Eating Behavior Questionnaire. Wanting to eat in response to environmental food cues was measured with the "external eating" scale of the Dutch Eating Behavior Questionnaire. Maximum-likelihood structural equation modeling was used to establish underlying common genetic and environmental influences.ResultsThere were significant positive phenotypic correlations between all traits except for reward responsiveness and BMI. Genetic factors explained the majority of the association between food responsiveness and external eating (74%, 95% CI: 61, 87), whereas common shared environmental factors explained the majority of the associations between reward responsiveness with both food responsiveness (55%, 95% CI: 20, 90) and external eating (70%, 95% CI: 39, 100).ConclusionsOur study demonstrates the importance of common environmental factors in the shared etiology between reward responsiveness and childhood eating behaviors. However, the common etiology underlying both reward responsiveness and BMI is unclear, as there was no phenotypic correlation between reward responsiveness and BMI at this age. Further longitudinal research needs to detangle this complex relationship throughout development.

Dataset Information

Parental substance use and child reward-driven eating behaviors.

Publications

Parental substance use and child reward-driven eating behaviors.

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