The Stress of Cold Temperatures Extends Lifespans

In 1986, John Holloszy of Washington University immersed his lab rats in shallow, cool water for four hours each day. They burned so many extra calories that they ate half again as much as control rats, but weighed less. The cold rats lived 10% longer, on average. Holloszy framed his report on this experiment not as a hormetic effect of cold exposure, but as a refutation of the “rate of living” hypothesis.

In 2006, Gordon Lithgow of the Buck Institute for Aging Research exposed lab worms to repeated heat shocks, and they lived 10-20% longer. Lithgow’s group noted that in response to the treatments the worms generated a surge of a protective hormone dubbed heat shock protein, and that heat shock protein also increases life span. They matter-of-factly reported their results as an example of hormesis, demonstrating that between 1986 and 2006, the concept of hormesis had worked its way into the field and become commonly integrated into gerontologists’ thought process.

Hormesis is the name for the paradoxical adaptation that makes animals live longer when they are exposed to challenges and hardships. Starvation, various toxins in low doses, infections, heat and cold can all lead to a longer life . These are not merely quirks of the physiology, but deep and ancient adaptations for the purpose of stabilizing population. The population death rate, like everything else about life, is homeostatic. That means that when something in the environment – perhaps a famine or an epidemic – is killing off part of the population, the rest of the population responds by toughening up and living longer. At the individual level, this is manifested as a slow-down of the aging process when starvation or other hardship is sensed. The response is managed by a logic system that works very much like a computer, but it is based on a web of hormones and chemical signals, in addition to neural circuits.