...patterns from influenza in the 1st 1/2 of the 20th century and the rise & fall of heart disease

[Hannah Bell]

Abstract

The classic risk factors for developing coronary heart disease (CHD) explain less than 50% of the decrease in mortality observed since 1950.

The transition currently under way, from the degenerative to the infectious-inflammatory paradigm, requires a new causal interpretation of temporal trends.

The following is an ecological study based on data from the United States showing that in men and women an association between the age distribution of mortality due to influenza and pneumonia (I&P) associated with the influenza pandemic in 1918-1919 in the 10-49-year age bracket and the distribution of CHD mortality from 1920 to 1985 in survivors from the corresponding birth cohorts.

It further shows a significant negative correlation (r = -0.68, p = 0.042) between excess mortality from I&P accumulated in epidemics from 1931 to 1940 (used as indicator for persistent circulation of H1N1 virus combined with vulnerability to infection) and the order of the beginning in the decline in CHD mortality in nine geographic divisions in the United States.

In light of current biological knowledge, the data suggest that the 1918 influenza pandemic and the subsequent epidemics up to 1957 might have played a determinant role in the epidemic of CHD mortality registered in the 20th century.

http://www.scielosp.org/scielo.php?script=sci_arttext&pid=S0102-311X2002000300002&lng=en&nrm=iso


In the course of the last 70 years, a rise and fall in mortality from coronary heart disease (CHD) occurred in several countries. In the United States, angina emerged as a significant cause of death in the mid-1920s (Stallones, 1980). From then on, CHD mortality rose steadily until the early 1960s, when it leveled off at around 35% of overall mortality (Havlick & Feinleib, 1979). The decline began in 1968 and accelerated after 1972 (Levi, 1981), resulting in a fall of more than 40% in CHD death rates in the last 30 years (Sytkowski et al., 1996).

The CHD mortality time trend has still not been explained satisfactorily (Metha et al., 1998), with traditional risk factors accounting for less than 50% of the variation in rates registered since 1950
...

Though speculative, a mechanism involving cross-reactivity between the H1N1 influenza strains and apoB-LDL or the LDL receptor could be a link from infection to hypercholesterolemia and CHD mortality and shed new light on the "diet-heart" controversy (Blackburn & Jacobs, 1984). Within populations, the effect of dietary fat/cholesterol intake on serum cholesterol levels might depend more on the efficiency of LDL uptake, the latter possibly influenced by a cross-reactive immune response to a previous H1N1 influenza infection.

In short, although biological links between influenza and CHD remain to be proven, intriguing leads do exist.