Thank you, Maria, that's helpful.

C

Maria Inês Reinert Azambuja wrote:
> I would like to disagree with this comon-sense idea of multiple 
> causes. To my understanding, this just reflecta our ignorance about 
> diseases causality.
> I have been trying to make this point with CHD causation. It is not so 
> much multiple risk fators as it is multiple diseases (CHDs), which 
> present at the population level as combination of  rates, each rate 
> resulting from an interaction between a the level of particular 
> environental exposure AND the historically built vulnerability 
> (inherited and acquired in the lifecourse) to the correspondent 
> exposure at that given point in time.
> In the case of CHD, I suggeted that the hipercholesterolemic cases 
> associated with high rates of mortality in the 19150s and 1960s 
> resulted from a 1918 Influenza Priming of vulnerable cohorts - those 
> that showed the higest mortality in 1918 - which set the stage of 
> vulnerability that resulted in CHD deaths due to coronary trombosis 
> during the 1950s and 1960s influenza epidemicas. CHD cases today belog 
> mostly to the pull of insulin-resistance cases. Those coursing with 
> hypercholesterolemia should be investigated regarding infection and 
> auto-immunity.
> (see 
> http://muse.jhu.edu/login?uri=/journals/perspectives_in_biology_and_medicine/v050/50.2azambuja.html 
>
>
> Obesity shoul also be called obesities.
> There are several conditions associated with this phenotype. The 
> epidemic type, as it occurred with CHD, possibly depended not as much 
> on a change in the environmental exposure as on a change in the 
> population vulnerability to that exposure. We need to look for the 
> determinant of vulnerability to understand the epidemic.
>
> Maria Inês
>

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