LAUSR

Biological mechanisms are ubiquitous in reports of epidemiological research. Many researchers extensively elaborate on a biological potential mechanism underlying their findings under the assumption that the presence of one is somehow related to the quality of their work. This interesting phenomenon echoes the work of Austin Bradford Hill, the famous epidemiologist who coined the Hill’s criteria for judgement of causality in epidemiological research. In Hill’s own words they are criteria from all of which “we should study association before we cry causation” [1]. They include strength, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment and analogy. All Hill’s criteria are almost never systematically used to judge whether associations represent causal effects. Hill’s plausibility criterion, however, is still frequently used to strengthen or weaken causal claims in epidemiological studies. Höfler phrased this criterion as “the observed association can be plausibly explained by substantive matter (e.g. biological) explanations” [2]. The exact definition of the term “mechanism” is topic of ongoing philosophical debate. In this viewpoint we define a mechanism of a behavior as “a complex system which produces that behavior by the interaction of a number of parts” as proposed by Glennan [3]. For the sake of the argument, we make a somewhat arbitrary distinction between “biological mechanisms” taking place within individual organisms, in contrast with “social” mechanisms that occur to populations [4]. While reading epidemiological reports, one cannot help feeling that epidemiologists highly value these biological mechanisms. Why is that and is it always justified?