The demographics of our planet have taken a turn towards rapid growth of older adult population. Predictions for 2050 indicate that 2 billion people on earth will be older than 60–65, the age at or near which most countries classify their citizens as seniors. With that population boom looming, it is incumbent upon societies to deal with issues and problems of older age, including increasing costs of health care.

While the precise molecular and cellular causes of aging remain elusive and often misnamed [1], it is clear that aging can be significantly postponed by several manipulations that affect nutrient sensing and cellular metabolism in a wide variety of model organisms, from yeast, worms and flies to rodents and perhaps primates [1–3]. These include nutritional manipulations (caloric restriction), pharmacological inhibition of the (mammalian) target of rapamycin (TOR/mTOR) or genetic attenuation or abrogation of growth factor (particularly insulin growth factor–IGF) pathways. Strikingly, these manipulations also seem to improve “Healthspan”, defined as reduced morbidity and mortality due to major age-related diseases, and ostensibly improved quality of life in older ages–at least under laboratory-controlled conditions. Henceforth emerge two key implications. First, it is likely that the fundamental cause of cellular aging lies, at least in part, in metabolic alterations. Second, successful intervention at the level of global Healthspan extension (the Holy Grail of gerontology) seems within reach for biomedical scientists studying the biology of aging.