It may well be that treatment choices will be better supported by evidence relating signs and symptoms (syndromes) to outcomes, rather than finding better ways of making a precise etiological or anatomical diagnosis.
The etiological approach interprets the teleological language of biology in much the same way Kant did i.e., as essentially metaphorical.
Regarding the way dementia was defined, no distinction was made between the different etiological types of dementia, and there can be differences between the comorbidities associated with each one of them [ 8].
These tales are now viewed as etiological — that is, they were invented to explain how the world got to be the way it is.
A possible way of resolving the inconsistencies is to incorporate nonadditive interactions between genes in an etiological model.
Additional uncertainties of a more fundamental nature also play a role: how to factor into such estimates the possibility (or indeed strong likelihood) that multiple risk factors interact in ways that we do not understand, thereby preventing a simple summing of the etiological contributions of different causes.
By way of example, we summarize our ongoing analyses of dopaminergic polymorphisms, as well as infectious etiological factors in schizophrenia genesis.
With conventional multi-stage regression models, all three of the "stage1" etiological factors (hookworm, HIV and vitamin A deficiency) would have to be assumed to be influencing (in some way) all four of the "stage 2" factors (iron deficiency, vitamin B12 deficiency, bacteraemia and malaria).
Still, a way to define distinct phenotypes of OA could be based on the main risk factors and etiological factors [ 12].
It is increasingly acknowledged that an important way forward is to invest in studies aimed at identifying genetically sensitive biological makers that relate to etiological processes, treatment response, and longer-term outcomes (Goodyer et al. 2010).
