Dec. 27, 2005 Records from four European countries show that, on average, survivors of generations with rampant childhood infection - measured by cohort mortality rates at young ages - were shorter and died sooner than counterparts from generations with less childhood disease.
Crimmins and Finch propose that even when they grew into apparently healthy adults, survivors of high-infection generations carried a heavier lifetime burden of inflammation. This in turn accelerated the progress of cardiovascular disease.
The authors also cited contemporary studies showing that respiratory infections, childhood diarrhea, dysentery and other common infectious diseases reduce growth.
When rates of infection dropped due to improved public health practices, adult survivors grew taller and lived longer.
"Our model implies that the reduction in lifelong levels of infections and inflammation reduced and delayed the progression of cardiovascular disease and mortality due to heart disease and allowed for increased height," said Crimmins, the study's lead author.
Other obvious beneficial factors, such as improved nutrition and higher standards of living, did not explain all the mortality data. Crimmins and Finch found that increases in height did not always follow improvements in income and nutrition. In addition, height decreased during some periods of improving income in early industrial cities.
The authors concluded that a reduction in infection and resulting inflammatory load had the potential to increase height independently of improved food intake.
This study extends previous research by Finch and Crimmins, published last year in the journal Science, that linked childhood infectious disease exposure to chronic inflammation leading to cardiovascular disease and a shortened lifespan.
For their current study, the authors collected mortality data from Sweden, France, England and Switzerland. The data begins in different years for each country but ends uniformly with individuals born in 1899.
After 1900, modern medicine became a dominant force in treating childhood illnesses, swamping the mortality effects studied by Crimmins and Finch.
"The inflammatory mechanism for our model only works when mortality from infection is high," Finch said. "Once childhood infection is low, it can no longer be a factor in explaining old-age trends."
Next, Crimmins and Finch plan to explore the possibility that the mechanisms of infection and aging in historical populations may apply to developing countries with high levels of infectious diseases and inadequate medical care.
This research was supported by the National Institute on Aging.
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