Cataract is the leading cause of blindness in the world, accounting for approximately 42% of all blindness. 1 Surgical treatment of cataracts imposes a substantial economic burden on health systems. Since cataract is primarily a disease of old age, we are facing a looming cataract epidemic in which the demand for cataract surgery will place greater demands on the resources available for treatment. An alternative approach to surgery is the development of therapies designed to prevent or delay the onset of cataract. It is therefore not surprising that the ultimate goal of many international lens research groups is to determine the causes of lens cataract, with a view toward developing novel anticataract therapies. A major obstacle to achieving this laudable goal is our current understanding of how the normal lens maintains its transparency. It has been proposed that the lens operates an internal microcirculation system that contributes to lens transparency by delivering nutrients to, and removing metabolic wastes from, the deep fiber cells while maintaining steady state lens volume (the lens fluid circulation model [FCM]). 2–4 Key features of the model remain to be tested. Such scientific debate is a normal and healthy component of the research discovery process, but the lack of an accepted understanding of lens physiology is compromising progress toward the ultimate goal of developing targeted anticataract therapies.

The purpose of the two perspectives presented in Point/Counterpoint is to formalize this debate. Evidence for and against the FCM will be presented, with the goal of identifying areas of future experimentation that are needed to test its validity. A general overview of the model is provided, followed by a summary of the evidence supporting it by Richard Mathias, Paul Donaldson, and Linda Musil. In the Counterpoint, David Beebe and Roger Truscott present a critique of the model. These articles are followed by brief rebuttals that summarize the critical experiments needed to test the model.