Ann Epidemiol. 2013 Dec;23(12):743-9. doi: 10.1016/j.annepidem.2013.09.001.
In this manuscript, I share insights into causal concepts that emerged from creating and refining a simple example originally designed for teaching causal epidemiologic concepts.
The insights that emerged are primarily related to the difference between how a causal effect occurs in an individual and what our methods assume about how a causal effect occurs when we estimate its effect in a population. In an individual, the causal effect of exposure on disease occurrence results from the interaction of several causal factors in that individual, not from a single factor in isolation. The result of this interaction within an individual determines an individual’s causal type (e.g., doomed, exposure causative, exposure preventive, immune) with respect to a particular exposure contrast and target (etiologic) time period. In a population, the causal effect of exposure on disease frequency depends on the distribution of causal types of individuals in that population, not necessarily on the population distribution of covariates. Yet in epidemiology, when we attempt to estimate the effect of a potential cause of interest, we (through the methods we use) usually do not account for this within individual causal interaction.
This failure to account for within-individual causal interactions has interesting implications for causal inference, as I illustrate here: (1) an effect estimate can be simultaneously confounded and unconfounded, (2) there can be confounding even if no variables satisfy the traditional criteria for being considered a confounder, (3) there can be no confounding even if there are variables that do satisfy the traditional confounder criteria, (4) the magnitude of confounding caused by a variable need not depend on the strength of the exposure-variable association, (5) a directed acyclic graph does not always correctly identify the presence of confounding, (6) the common-cause confounder criterion is imperfect, and (7) a time-varying confounder does not necessarily lead to time-varying confounding.
Our example illustrates that confounding is a “team sport”: single variables do not confound by themselves; confounding depends on how variables interact in individuals, not just on how variables are distributed within and across populations. Because confounding depends on how variables interact in individuals, methods that ignore causal interactions in individuals are not guaranteed to be confounding identification methods.
在本文中,我分享了从创建和精炼最初设计用于教授因果流行病学概念的简单示例中得出的因果概念的见解。
出现的见解主要与因果效应在个体中发生的方式与我们在估计人群中因果效应时对因果效应发生方式的假设之间的差异有关。在个体中,暴露对疾病发生的因果效应源自该个体中几个因果因素的相互作用,而不是单个因素的孤立作用。这种个体内相互作用的结果决定了个体相对于特定暴露对比和目标(病因)时间段的因果类型(例如,命中注定、暴露因果、暴露预防、免疫)。在人群中,暴露对疾病频率的因果效应取决于该人群中个体因果类型的分布,而不一定取决于人群中协变量的分布。然而,在流行病学中,当我们试图估计感兴趣的潜在原因的效果时,我们(通过我们使用的方法)通常不会考虑个体内因果相互作用。
这种未能考虑个体内因果相互作用对因果推断具有有趣的影响,正如我在这里说明的那样:(1)效应估计可以同时存在混杂和非混杂,(2)即使没有变量满足被认为是混杂因素的传统标准,也可能存在混杂,(3)即使存在满足传统混杂因素标准的变量,也可能不存在混杂,(4)变量引起的混杂程度不一定取决于暴露变量的关联强度,(5)有向无环图并不总是正确识别混杂的存在,(6)共同原因混杂因素标准不完美,以及(7)时变混杂因素不一定导致时变混杂。
我们的示例表明,混杂是一项“团队运动”:单个变量本身不会混杂;混杂取决于变量在个体中的相互作用方式,而不仅仅是变量在人群内和人群间的分布方式。由于混杂取决于变量在个体中的相互作用方式,因此忽略个体中因果相互作用的方法不一定是混杂识别方法。