Although aging is ubiquitous across organisms, the rate at which it occurs varies considerably between species and individuals. The initial links between oxidative stress and rates of cellular aging were postulated over 50 years ago by Harman, who published a theory connecting free radical damage with the aging process in 1956 1 . Since then a wide body of literature has accumulated demonstrating the links between oxidative damage to various cellular components and cellular senescence 2 . Oxidative stress is known to contribute to the aetiology of a wide variety of pathological processes including metabolic, cardiovascular and neoplastic diseases, all of which can shorten lifespan. Macromolecules such as proteins, lipids and particularly DNA can be irreversibly damaged by oxidative stress, leading to a decline in cellular function and apoptosis. This leads to aging, initially at a cellular level, then of the tissues and organs, culminating in whole organism pathology and eventually death. This article explores the various processes by which cells accrue oxidative damage and how such long-term damage leads to senescence. In particular, we focus on how the early-life environment influences the accumulation of oxidative stress over the entire life-course of an individual and how this may accelerate the normal aging process.