Golan Daniel, Linn Shay
Harefuah. 2015 Jun;154(6):389-93, 403.
The pathogenesis of most chronic diseases is complex and probably involves the interaction of multiple genetic and environmental risk factors. One way to learn about disease triggers is from statistically significant associations in epidemiological studies. However, associations do not necessarily prove causation. Associations can commonly result from bias, confounding and reverse causation. Several paradigms for causality inference have been developed. Henle-Koch postulates are mainly applied for infectious diseases. Austin Bradford Hill's criteria may serve as a practical tool to weigh the evidence regarding the probability that a single new risk factor for a given disease is indeed causal. These criteria are irrelevant for estimating the causal relationship between exposure to a risk factor and disease whenever biological causality has been previously established. Thus, it is highly probable that past exposure of an individual to definite carcinogens is related to his cancer, even without proving an association between this exposure and cancer in his group. For multifactorial diseases, Rothman's model of interacting sets of component causes can be applied.
大多数慢性病的发病机制很复杂,可能涉及多种遗传和环境风险因素的相互作用。了解疾病触发因素的一种方法是通过流行病学研究中具有统计学意义的关联。然而,关联并不一定证明因果关系。关联通常可能源于偏倚、混杂和反向因果关系。已经开发了几种因果推断范式。亨勒-科赫假设主要应用于传染病。奥斯汀·布拉德福德·希尔准则可作为一种实用工具,用于权衡关于给定疾病的单一新风险因素确实具有因果关系的可能性的证据。每当先前已经确立生物学因果关系时,这些准则对于估计暴露于风险因素与疾病之间的因果关系就无关紧要了。因此,即使没有证明个体过去接触特定致癌物与他所在群体中的癌症之间存在关联,个体过去接触特定致癌物与他患癌症之间很可能存在关联。对于多因素疾病,可以应用罗斯曼的组分病因相互作用模型。