Using mathematical modeling, researchers at New York and Vanderbilt universities have shown that commensal bacteria that cause problems later in life most likely played a key role in stabilizing early human populations. The finding, published in mBio®, the online open-access journal of the American Society for Microbiology, offers an explanation as to why humans co-evolved with microbes that can cause or contribute to cancer, inflammation, and degenerative diseases of aging. The work sprung from a fundamental question in biology about senescence, or aging past the point of reproduction. "Nature has a central problem--it must have a way to remove old individuals, whether fish or trees or people," says Martin Blaser, microbiologist at New York University Langone Medical Center in New York City. "Resources are always limited. And young guys are ultimately competing with older ones."

In most species, individuals die shortly after the reproductive phase. But humans are weird--we have an extra long senescence phase. Blaser began to think about the problem from the symbiotic microbe's point of view and he came up with a hypothesis: "The great symbionts keep us alive when we are young, then after reproductive age, they start to kill us." They are part of the biological clock of aging.

In other words, he hypothesized that evolution selected for microbes that keep the whole community of hosts healthy, even if that comes with a cost to an individual host's health.

Modeling of early human population dynamics could tell him if he was on the right track. Blaser worked together with his collaborator Glenn Webb, professor of mathematics at Vanderbilt University in Nashville, to define a mathematical model of an early human population, giving it characteristics similar to a time 500-100,000 years ago, when the human population consisted of sparse, isolated communities.