Building causal knowledge in behavior genetics

被引:26
作者
Madole, James W. [1 ,2 ]
Harden, K. Paige [1 ]
机构
[1] Univ Texas Austin, Dept Psychol, Austin, TX 78712 USA
[2] VA Puget Sound Hlth Care Syst, Seattle, WA USA
关键词
behavior genetics; causal inference; counterfactual reasoning; experimental designs; individual differences; philosophy of science; GENOME-WIDE ASSOCIATION; POLYGENIC RISK; HAPLOTYPE BLOCKS; BIPOLAR DISORDER; ENVIRONMENT; HERITABILITY; INFERENCE; HETEROGENEITY; RECOMBINATION; CHILDHOOD;
D O I
10.1017/S0140525X22000681
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects.
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页数:57
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