Variation in attributes of CHD cases over time suggests a temporal change in the source sub-population of cases. It is proposed that an early 20th century expansion of a CHD-prone sub-population, characterized by high-serum cholesterol phenotype and high case-fatality - and which contributed with most of the CHD cases and deaths during the 1960s - may have followed the 1918 Influenza Pandemic. The extinction of those birth-cohorts would have resulted in a relative increase in cases coming from a second source sub-population, characterized by insulin resistance and chronic expression of low grade inflammation markers, comparatively less vulnerable to acutely die from CHD. This re-interpretation of the CHD trend, and the abandonment of the idea of degeneration for inflammation/infection calls for a change in epidemiology. Besides exposures (diet, infection...), temporal variations in proportional representations of inherited and acquired phenotypes associated with individual resistance/vulnerability, would be important determinants of evolving patterns of diseases occurrences in populations.
Influenza; Heart disease; Epidemic; Mortality; Ecologic studies