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One of the main benefits of the dramatic technological progress over the last two centuries is the enormous increase in human life expectancy, which has now reached record highs. After conquering most childhood diseases and a fair fraction of the diseases that plague adulthood, medical technology is now mainly preoccupied by age-related disorders. Further progress is dependent on circumventing the traditional medical focus on individual diseases and instead targeting aging as a whole as the ultimate cause of the health problems that affect humankind at old age. In principle, a major effort to control the gradual accumulation of molecular and cellular damage - considered by many as the ultimate cause of intrinsic aging - may rapidly lead to interventions for regenerating aged and worn-out tissues and organs. While considered impossible by many, there really is no reason to reject this as scientifically implausible. However, as we posit, it is not only scientific progress that is currently a limiting factor, but societal factors that hinder and may ultimately prevent further progress in testing and adopting the many possible interventions to cure aging.

Much research interest, and recently even commercial interest, has been predicated on the assumption that reasonably closely-related species – humans and mice, for example – should, in principle, respond to ageing-retarding interventions with an increase in maximum lifespan roughly proportional to their control lifespan (that without the intervention). Here, it is argued that the best-studied life-extending manipulations of mice are examples of a category that is highly unlikely to follow this rule, and more likely to exhibit only a similar absolute increase in maximum lifespan from one species to the next, independent of the species’ control lifespan. That category – reduction in dietary calories or in the organism’s ability to metabolize or sense them – is widely recognized to extend lifespan as an evolutionary adaptation to transient starvation in the wild, a situation which alters the organism’s optimal partitioning of resources between maintenance and reproduction. What has been generally overlooked is that the extent of the evolutionary pressure to maintain adaptability to a given duration of starvation varies with the frequency of that duration, something which is – certainly for terrestrial animals and less directly for others – determined principally by the weather. The pattern of starvation that the weather imposes is suggested here to be of a sort that will tend to cause all terrestrial animals, even those as far apart phylogenetically as nematodes and mice, to possess the ability to live a similar maximum absolute (rather than proportional) amount longer when food is short than when it is plentiful. This generalization is strikingly in line with available data, leading (given the increasing implausibility of further extending human mean but not maximum lifespan in the industrialized world) to the biomedically and commercially sobering conclusion that interventions which manipulate caloric intake or its sensing are unlikely ever to confer more than 2 or 3 years’ increase in human mean or maximum lifespan at the most.

In their article in this issue, Olshansky and Carnes [Gerontology 2013;59:85–92] spell out in perhaps the most explicit terms yet a view which they have long espoused: that increases in longevity will inevitably slow down in decades to come, since the rate of biomedical progress that everyone agrees would be necessary to avoid such a slowdown is far too dramatic to be plausible. By doing so, they also betray more explicitly than ever before the flaws in their own logic. It is ironic that these flaws, unlike the work they critique, are actually quite closely analogous to the flaws in Zeno’s paradox. Since others are offering their own comments on other parts of the article, I shall restrict my remarks on the article to those passages which refer specifically to my own work, together with the conclusion.