[FROM STATISTICAL ASSOCIATIONS TO SCIENTIFIC CAUSALITY].
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.
Daniel
D
Golan
Shay
S
Linn
D015982:Bias; D002273:Carcinogens / Q000633:toxicity; D015984:Causality; D002908:Chronic Disease; D004781:Environmental Exposure / Q000009:adverse effects*; D004812:Epidemiologic Methods; D020022:Genetic Predisposition to Disease; D006801:Humans; D009369:Neoplasms / Q000453:epidemiology / Q000209:etiology; D011336:Probability; D012307:Risk Factors
D002273:Carcinogens