There is growing evidence to support a role for leptin resistance in inducing or driving OHS.[42–46] In a recent paper by Campo et al., a total of 245 obese subjects underwent detailed testing, and it was found that hyperleptinemia was associated with a reduction in respiratory drive and hypercapnic response, irrespective of the amount of body fat, which suggests the extension of leptin resistance to the respiratory center.[47] Various forms of SDB have been implicated in the pathogenesis of OHS, including OSA, central hypoventilation and upper airway resistance syndrome. This evidence concerns the gene LEP and sleep apnea syndrome.