By 2050, the number of people over the age of 80 will triple globally. These demographics could come at great cost to individuals and economies.
The problems of old age come as a package. More than 70% of people over 65 have two or more chronic conditions such as arthritis, diabetes, cancer, heart disease and stroke.
Restricting calorie intake in mice or introducing mutations in nutrient-sensing pathways can extend lifespans by as much as 50%. And these ‘Methuselah mice’ are more likely than controls to die without any apparent diseases.
The current tools for extending healthy life — better diets and regular exercise — are effective. But there is room for improvement, especially in personalizing treatments.
Longevity pathways identified in model organisms seem to be conserved in humans and can be manipulated in similar ways. Genetic surveys of centenarians implicate hormonal and metabolic systems. Long-term calorie restriction in humans induces drastic metabolic and molecular changes that resemble those of younger people, notably in inflammatory and nutrient-sensing pathways.
Several molecular pathways that increase longevity in animals are affected by approved and experimental drugs. Cancer and organ-rejection drugs such as rapamycin extend lifespan in mice and worms by muting the mTOR pathway, which regulates processes from protein synthesis to cell proliferation and survival. The sirtuin proteins, involved in a similar range of cellular processes, are activated by high concentrations of naturally occurring compounds (such as the resveratrol found in red wine) and extend lifespan in metabolically abnormal obese mice. A plethora of natural and synthetic molecules affect pathways that are shared by ageing, diabetes and metabolic syndrome. (Luigi Fontana, Brian K. Kennedy, Valter D. Longo, Douglas Seals& Simon Melov, Nature 511, 405–407 (24 July 2014) doi:10.1038/511405a)