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We describe the principles of counterfactual thinking in providing more precise definitions of causal effects and some of the implications of this work for the way in which causal questions in life course research are framed and evidence evaluated. Terminology is explained and examples of common life course analyses are discussed that focus on the timing of exposures, the mediation of their effects, observed and unobserved confounders, and measurement error. The examples are illustrated by analyses using singleton and twin cohort data.

IMPORTANCE: The early obesogenic home environment is consistently identified as a key influence on child weight trajectories, but little research has examined the mechanisms of that influence. Such research is essential for the effective prevention and treatment of overweight and obesity. OBJECTIVE: To test behavioral susceptibility theory’s hypothesis that the heritability of body mass index (BMI) is higher among children who live in more obesogenic home environments. DESIGN, SETTING, AND PARTICIPANTS: This study was a gene-environment interaction twin study that used cross-sectional data from 925 families (1850 twins) in the Gemini cohort (a population-based prospective cohort of twins born in England and Wales between March and December 2007). Data were analyzed from July to October 2013 and in June 2018. EXPOSURES: Parents completed the Home Environment Interview, a comprehensive measure of the obesogenic home environment in early childhood. Three standardized composite scores were created to capture food, physical activity, and media-related influences in the home; these were summed to create an overall obesogenic risk score. The 4 composite scores were split on the mean, reflecting higher-risk and lower-risk home environments. MAIN OUTCOMES AND MEASURES: Quantitative genetic model fitting was used to estimate heritability of age-adjusted and sex-adjusted BMI (BMI SD score, estimated using British 1990 growth reference data) for children living in lower-risk and higher-risk home environments. RESULTS: Among 1850 twins (915 [49.5%] male and 935 [50.5%] female; mean [SD] age, 4.1 [0.4] years), the heritability of BMI SD score was significantly higher among children living in overall higher-risk home environments (86%; 95% CI, 68%-89%) compared with those living in overall lower-risk home environments (39%; 95% CI, 21%-57%). The findings were similar when examining the heritability of BMI in the separate food and physical activity environment domains. CONCLUSIONS AND RELEVANCE: These findings support the hypothesis that obesity-related genes are more strongly associated with BMI in more obesogenic home environments. Modifying the early home environment to prevent weight gain may be particularly important for children genetically at risk for obesity.