Starting in the mid-1850s, humans began living longer due, researchers believe, to improvements in living conditions, nutrition, income levels and medicine.
But two USC gerontologists have found an invisible cause that could have important implications for modern-day health care.
In a paper published in the Sept. 17 issue of the journal Science, Caleb Finch and Eileen Crimmins firmly link this gradual yet steady increase in human life span to lower childhood rates of exposure to infectious diseases such as tuberculosis and malaria.
The key to their theory lies in one word: inflammation.
Infectious diseases cause chronic inflammation in the blood that, decades later, leads to heart attacks, strokes and cancers – the classic killers of old age.
"We've put pieces together that are in front of everybody's nose and made a coherent hypothesis," said Caleb Finch, the study's lead author and holder of the ARCO-William F. Kieschnick Chair in the Neurobiology of Aging.
"Our main point is that in historical times when there was a lot of childhood mortality, even kids that didn't die got chronic infections. Those chronic infections from childhood onward accelerated vascular and other diseases," he said.
Finch and Crimmins, holder of the Edna M. Jones Chair in Gerontology, studied data on the health and mortality rates of people born in Sweden from 1751 to 1940. Grouping them by birth year – into what are called birth cohorts – the researchers found that as public health efforts led to less exposure to infectious diseases during childhood, people started living longer and better.
"Most people have been looking for an explanation for health change among the old in current conditions," Crimmins said. "We're saying that part of the roots of health in old age lie in childhood. That is what makes this study different because we started looking at the person and their living conditions at a much younger age than other studies."
Finch said the study's findings are consistent with observations that modern-day drugs that fight inflammation also reduce the risk of cardiovascular disease and possibly Alzheimer's.
Drug treatments might potentially be started much earlier, Finch said. Children found to be genetically predisposed to heart disease, for example, could be treated starting at a much younger age.
"These people would have a special lifestyle recommendation from the earliest years," Finch said. "We noticed that improvements in the environment may be reaching a maximum which would mean that further increase in life expectancy will depend on interventions other than public health such as this new generation of drugs."