Model organism lifespan research

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The body of work in which lifespan is manipulated in short-lived laboratory species — chiefly the nematode Caenorhabditis elegans, the fruit fly Drosophila melanogaster, and laboratory mice — and from which almost every mechanistic claim about ageing originates. The results are genuinely dramatic: single-gene mutations in the insulin/IGF-1 signalling pathway more than double nematode lifespan, and dietary or pharmacological interventions extend mouse lifespan by measurable percentages. The translation record is the problem. Effects shrink monotonically with organism complexity and lifespan — a doubling in a worm becomes tens of percent in a fly, ten to twenty percent in a mouse, and nothing demonstrated in a human. Laboratory rodents are inbred, live in pathogen-free cages on ad libitum diets, and die predominantly of cancer, so a compound that extends their lifespan may be doing something about their specific failure mode rather than about ageing. Reading a mouse result as a human one is the single most common error in this field.

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