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Sibling Fixed-Effects Design×Life-Course Epidemiology×
분야Social EpidemiologySocial Epidemiology
계열Regression modelProcess / pipeline
기원 연도20132002
창시자Brian D'Onofrio, Benjamin Lahey, Eric Turkheimer & Paul Lichtenstein; Thomas Frisell et al.Yoav Ben-Shlomo & Diana Kuh
유형Within-family fixed-effects design for confounding controlConceptual and analytic framework for long-term exposure-disease modeling
원전Frisell, T., Oberg, S., Kuja-Halkola, R., & Sjolander, A. (2012). Sibling Comparison Designs: Bias From Non-Shared Confounders and Measurement Error. Epidemiology, 23(5), 713-720. DOI ↗Ben-Shlomo, Y., & Kuh, D. (2002). A life course approach to chronic disease epidemiology: conceptual models, empirical challenges and interdisciplinary perspectives. International Journal of Epidemiology, 31(2), 285-293. DOI ↗
별칭Sibling Comparison Design, Within-Family Fixed Effects, Discordant Sibling Design, Discordant Twin DesignLife Course Approach to Chronic Disease, Life-Course Framework, Developmental Origins Epidemiology, Biological and Social Programming Approach
관련43
요약The sibling fixed-effects, or sibling-comparison, design controls for everything that siblings share by construction. Genes (on average half), parents, household income, neighborhood, schooling, and family culture are differenced out when you compare brothers or sisters who differ in an exposure, so the residual within-family association is purged of all confounders common to the family. D'Onofrio, Lahey, Turkheimer, and Lichtenstein championed these family-based quasi-experiments as a way to integrate genetic and social-science research by rigorously testing competing causal hypotheses. Frisell and colleagues, however, gave the design its essential warning label: precisely because shared confounding is removed, the within-family estimate is unusually vulnerable to the confounders siblings do not share and to attenuation from measurement error. The design is powerful but double-edged.Life-course epidemiology is the study of how physical and social exposures across gestation, childhood, adolescence, and adult life shape later health and disease risk. Codified by Yoav Ben-Shlomo and Diana Kuh in their 2002 International Journal of Epidemiology paper and the 2003 glossary by Kuh, Ben-Shlomo, Lynch, Hallqvist, and Power, the framework supplies a set of competing conceptual models that specify how the timing and sequence of exposures matter. Rather than asking only what causes disease, it asks when exposures act and how their effects compound. Its three signature models — critical or sensitive periods, accumulation of risk, and chains of risk — give researchers a disciplined way to translate developmental and social theory into testable longitudinal hypotheses about the origins of adult chronic disease.
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