Things happen faster when it’s warmer. This is true all the way down to the molecular level: many chemical reactions are accelerated at increased temperature. This leads to a fairly straightforward potential explanation for the longstanding observation that among organisms that are unable to regulate their own body temperature, higher temperature means a shorter lifespan — namely, the biochemical changes that underlie aging are simply happening faster.
This is probably true to some extent, but it’s not the whole story. A study by Lee and Kenyon reveals that there is active bioregulation of lifespan in response to temperature:
Many ectotherms, including C. elegans, have shorter life spans at high temperature than at low temperature. High temperature is generally thought to increase the “rate of living” simply by increasing chemical reaction rates. In this study, we questioned this view and asked whether the temperature dependence of life span is subject to active regulation.
We show that thermosensory neurons play a regulatory role in the temperature dependence of life span. Surprisingly, inhibiting the function of thermosensory neurons by mutation or laser ablation causes animals to have even shorter life spans at warm temperature. Thermosensory mutations shorten life span by decreasing expression of daf-9, a gene required for the synthesis of ligands that inhibit the DAF-12, a nuclear hormone receptor. The short life span of thermosensory mutants at warm temperature is completely suppressed by a daf-12(-) mutation.
Our data suggest that thermosensory neurons affect life span at warm temperature by changing the activity of a steroid-signaling pathway that affects longevity. We propose that this thermosensory system allows C. elegans to reduce the effect that warm temperature would otherwise have on processes that affect aging, something that warm-blooded animals do by controlling temperature itself.
In other words, higher temperatures do indeed shorten lifespan, but they shorten them even more if the animal is unaware of the higher temperatures. Thermosensory neurons sense the adverse conditions and presumably activate a program that counteracts the life-shortening effects of a warmer environment.
Despite the rhetoric in the abstract, this doesn’t put an end to the “rate of living” hypothesis. There’s clearly a shortening of lifespan in response to elevated temperature; the existence of a pathway that limits that shortening doesn’t argue either way about the role (if any) played by the acceleration of biochemical reactions or cellular/systemic events at under warmer conditions.
So, then: what’s the mechanism of the relative lifespan extension conferred by thermosensory neurons? Still unknown, but given the well-funded lab group in question, I’d be surprised if an expression profiling experiment were far behind. My money is on heat shock proteins, regulated not in response to heat, but in response to neuroendocrine factors secreted by temperature-sensitive nerve cells.
Lee, S., & Kenyon, C. (2009). Regulation of the Longevity Response to Temperature by Thermosensory Neurons in Caenorhabditis elegans Current Biology DOI: 10.1016/j.cub.2009.03.041