Here's a Darwinian puzzle: cellular senescence excels at fending off cancer for the first 30 years of life. After that, the tables turn and it becomes a key player in promoting cancer and several other age-related pathologies. How could natural selection allow this to occur?
Don't blame evolution for this about-face. We're simply living too long, or at least much longer than the vast majority of generations that came before us. Today, it's not uncommon for people to live to 95. But for 99 percent of human evolution, our ancestors' lifespan was limited by disease, predators, hazards such as droughts and cold spells, and plain old hard living. You were lucky if you reached 30, which means that evolution only had to fight cancer for that long too.
In other words, the process that controls cellular senescence adheres to a carefully scripted playbook for the first 30 years of life. After that it improvises. And left to their own devices, senescent cells accumulate throughout the body and contribute to tissue degradation. This means those extra 65 years we've finagled through modern medicine, a steady food supply, and central heating come at a price, at least for now. We just have to wait a few hundred generations for evolution to catch up.
To learn more about such mysteries of how and why we age, Campisi and
colleagues have created the Center
for Research and Education in Aging. The multidisciplinary center
investigates the basic processes that cause aging, with the goal of improving
and extending human health span.