ABSTRACT
Obstructive sleep apnea (OSA) is a disease limited almost exclusively to humans. The only animal model for OSA is the English bulldog (1), which serves as a model for OSA secondary to craniofacial anomalies (midfacial hypoplasia), rather than the more common human condition of OSA secondary to obesity. Despite attempts to develop animal models of OSA related to obesity, even very obese animals, such as pigs or obese knockout mice, do not develop OSA. Why then, does this disease occur so often in humans? The human pharynx has several functions which compete with each other (2), including breathing (during which the pharynx must remain patent) and swallowing (during which the pharynx must collapse). Some unique characteristics of the human have affected the ability of the upper airway to perform these different functions: the ability of humans to perform complex speech, and the upright position of humans compared to quadrupedal animals. This inherent tendency for the human upper airway to collapse predisposes it to abnormal collapse during sleep, that is, obstructive apnea.
