Dietary restriction in Drosophila: delayed aging or experimental artefact?

Abstract

Lifespan can be extended by reduction of dietary intake. This practice is referred to as dietary restriction (DR), and extension of lifespan by DR is evolutionarily conserved in taxonomically diverse organisms including yeast, invertebrates, and mammals. Although these two often-stated facts carry the implication that the mechanisms of DR are also evolutionarily conserved, extension of lifespan could be a case of evolutionary convergence, with different underlying mechanisms in different taxa. Furthermore, extension of lifespan by different methods of DR in the same organism may operate through different mechanisms. These topics remain unresolved because of the very fact that the mechanisms of DR are unknown. Given these uncertainties, it is essential that work on the mechanisms of DR is not clouded by imprecise descriptions of methods or by technical problems. Here we review the recent literature on DR in Drosophila to point out some methodological issues that can obscure mechanistic interpretations. We also indicate some experiments that could be performed to determine if DR in Drosophila operates through similar mechanisms to the process in rodents.

Figure 1. The Responses of Lifespan and Fecundity to Food Concentration That Is Required for DR Studies in Drosophila

As food concentration increases from starvation, lifespan should increase to a peak at DR, from which it declines due to a nutrient-dependent effect of “high” food. If fecundity decreases (A) or is unchanged (B) by the nutrient increase that decreases lifespan, the most likely explanation for shortened lifespan is toxicity. To minimise the possibility that food toxicity is the explanation for the lifespan shortening at high food concentrations, it is important that daily and lifetime fecundity increase for the increases in food concentrations that decrease lifespan (C).