Eileen Crimmins
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Longer (and Taller) Lives
Centuries-Old Records Confirm Link Between Health and Lifespan
By Kirsten Holguin
Current life expectancy has reached an all time high of 77-plus years,
almost double the life expectancy of someone living 250 years ago.
Although modern medicine accounts for some of the increase in
mortality, it does not explain it all.
According to a new analysis of 18th and 19th century public
health records, high rates of childhood infection stunt growth and
accelerate aging.
The study by demographer Eileen Crimmins and neuroscientist Caleb
Finch, professors with joint appointments in USC College and the School
of Gerontology, expands upon the duo’s previous research, which
suggested that today’s longer life-spans may be partially explained by
lower rates of infectious disease in childhood.
The new study appeared Dec. 30 in the early online edition of the Proceedings of the National Academy of Sciences.
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 and holder of the Edna
M. Jones Chair in Gerontology.
Other obvious beneficial factors, such as improved nutrition and higher
standards of living, did not explain all the mortality decline. The USC
researchers found that increases in height did not always follow
improvements in income and nutrition. In addition, height decreased
during some periods of rising average 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, which 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,” said Finch, a University Professor and the
ARCO/William F. Kieschnick Chair in the Neurobiology of Aging. “Once
childhood infection is low, it can no longer be a factor in explaining
old-age trends.”
Crimmins and Finch believe it is possible 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.
The research was supported by the National Institute on Aging.
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