Everything should be made as simple as possible but not simpler

Rodolfo Saracci · International Journal of Epidemiology · 2006

Can complexity theory throw some different light on the aetiology of complex diseases,1 currently explored mostly by the probe of molecular genetics?2 Epidemiology, particularly as developing in the last half a century, has been dealing with disease aetiology—‘a priori’ not known whether simple or complex—with quite simple tools from an epistemological viewpoint. Observational epidemiology studies of aetiological factors are conceived, and whenever feasible carried out, as association studies at the individual level. An association and its nature, causal or non-causal, is researched within the same individuals of one or more exposures of interest with an outcome adjusting for other exposures, which may distort (confound) the association. This basic and invariant study concept has been developed into a vast and sound array of methods of study design and statistical analysis aimed at (i) making it applicable within a variety of purely observational circumstances and (ii) approaching the same study validity attainable by an experiment in which exposures are selected and assigned at will by the investigator and randomization is employed to control confounding and biasing factors unknown or known but not controlled by systematic arrangement.

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