modern variation and evolutionary change in the hominin eye orbit

one group and spread to all other areas within only a few thousand years, particularlybecause near-sightedness is selectively neutral.A genetic mutation that diminishes eyesight could only persist in a population thatdoes not rely extensively on acute vision for survival, or is capable of developing somemeans to physically correct the focal error; as a result it can only be in recent humanhistory that genes affecting visual acuity would be permitted to persist (Cordain et. al.2002; Miller, 1992). If there is a heritable genetic component to the pathogenesis ofmyopia a relaxation of selection pressure favoring individuals with keen eyesight wouldmake it possible for such a gene or genes to endure. However, even though visualdeterioration would be permitted in recent human history, a mutation affecting eyegrowth cannot be the only cause of juvenile-onset myopia, as this condition develops inhighly patterned ways and occurs at a very high rate in some populations but not others.The common pattern of myopia development and the many biological and socialcorrelates would not occur if myopia were a purely genetic abnormality.Most research investigating the etiology of juvenile-onset myopia has focused onthe eyeball as a relatively isolated unit, overlooking its close proximity to and spatialrelationship with surrounding extraocular tissues, the orbit, facial framework,neurocranium, and brain. As a result, the final section of this thesis examines therelationship between the eyeball and orbit, and how relative size of the globe within thebony orbit relates to the frequency and severity of myopic refractive error. This researchalso aims to provide a model for investigating reduced visual acuity in humans, andcontribute to an understanding of the degree to which modern variation and evolutionarychange in orbital and overall craniofacial morphology may explain the common eye form27