Evolution suggests that engineering an organism for immortality would not be desirable, even if it were possible, says Ernest Fraenkel, Professor of Biological Engineering. Aging, and eventually dying, is a consequence of the accumulation of damage to an organism over time. There is wear and tear on DNA, from chemicals in the environment, or radiation, or copying errors. Cells may not divide correctly, and proteins can misfold, leading to gradual deterioration of tissues, or catastrophic disease and system shutdown. Yet this sorry progression, says Fraenkel, has a logic: “The strategy that nature seems to use over and over is to let cells and organisms that have accumulated all this damage die off—and give their progeny a fresh start to go on and conquer the world.”
While evolution favored mortality, Fraenkel believes “there is no theoretical reason why organisms couldn’t have evolved to be immortal.” In fact, there are some that come awfully close, he notes. The bacterium Deinococcus radiodurans can survive terrible radiation damage and extremely cold, acidic conditions. There are also the “funky” Tardigrades, tiny invertebrates that seem immune to the effects of long periods of dehydration, heat, and even the vacuum of space.
Humans will probably never cheat death entirely, but our longevity has shot up in recent centuries (at least in more developed parts of the world), and current research may bring us even longer life spans. Fraenkel points to studies that suggest near-starvation diets can slow aging and age-related disease in many organisms by modifying the activity of specific proteins. Not surprisingly, researchers are looking for chemical compounds that can achieve the same impact “and allow us to at least age gracefully over longer periods,” Fraenkel says.
There are dangers associated with such elixirs, though. Humans that escape death and disease might still have age-associated changes in how they think and how they respond to disease. The compounds that ward off disease will also mess with other essential biological processes, preventing one disease and accelerating another. Fraenkel has taken an interest in these double-edged therapeutics in his work on Huntington’s disease, a rare neurodegenerative disorder. He is exploring ways to “dial up or dial down protein activity” to derive selective benefits without their associated costs. Fraenkel’s research could also reveal molecular pathways for constructive interventions in diseases associated with aging, such as Type 2 diabetes.
It is likely we will design drugs to extend our lifespan by 25 years or so in the not-distant future, Fraenkel says. But while he finds the prospect of becoming a supercentenarian “appealing on a personal and professional level,” he wonders which would be more socially responsible: “seeing if there are ways to extend life in the developed world, or eradicating infectious disease in the third world?” — Leda Zimmerman