Epidemiological evidence suggests there are significant links between obesity and obstructive sleep apnoea (OSA), with a particular emphasis on the importance of fat distribution in the development of OSA. In patients with OSA, the structure of the pharyngeal airway collapses. A collapsible tube within a rigid box collapses either due to decreased intraluminal pressure or increased external tissue pressure (i.e. reduction in transmural pressure), or due to reduction in the longitudinal tension of the tube. Accordingly, obesity should structurally increase the collapsibility of the pharyngeal airway due to excessive fat deposition at two distinct locations. In the pharyngeal airway region, excessive soft tissue for a given maxillomandibular enclosure size (upper airway anatomical imbalance) can increase tissue pressure surrounding the pharyngeal airway, thereby narrowing the airway. Even mild obesity may cause anatomical imbalance in individuals with a small maxilla and mandible. Lung volume reduction due to excessive central fat deposition may decrease longitudinal tracheal traction forces and pharyngeal wall tension, changing the ‘tube law’ in the pharyngeal airway (lung volume dependence of the upper airway). The lung volume dependence of pharyngeal airway patency appears to contribute more significantly to the development of OSA in morbidly obese, apnoeic patients. Neurostructural interactions required for stable breathing may be influenced by obesity-related hormones and cytokines. Accumulating evidence strongly supports these speculations, but further intensive research is needed.