Globally, 2.1 billion people are presbyopic, and 35 million are visually impaired due to cataract. With a rapidly ageing, and increasingly diabetic population, the extent of this burden will rise and increase the cost to the health system. While it is believed these two lens pathologies are linked by oxidative damage to lens proteins, antioxidant-based therapies have to date proven ineffective in slowing the onset of either presbyopia or cataract. Our confirmation of the existence of a lens microcirculation system, which generates a circulating flux of water, provides an alternative view to understand how oxidative damage leads to the onset of presbyopia and both age-related nuclear and diabetic cataract. By studying how water transport is regulated in the lens, we will develop novel antioxidant-based approaches to maintain the optical properties and transparency of the lens, and thereby prevent the onset of presbyopia and cataract.