Insomnia and OSA have been shown to contribute to an increased risk of several chronic health conditions (\citep*{Hargens2013} including, but not restricted to, diabetes mellitus \citep{Punjabi2004} and cardiovascular disease \cite{Somers2008}, asthma \citep{Janson1996}, systemic lupus erythematosus \citep{Gudbjörnsson2001}, rheumatoid arthritis \citep{Luyster2011} and inflammatory bowel disease \citep{Keefer2006}. Although there are many types of sleep disorders, most result in a reduction of sleep quality and duration which has been associated with increased body weight and adiposity \citep{López-García2008}\citep{Patel2008}. Although obesity has not yet be classified as a chronic condition in its own right in the UK, it has been formally recognised as such in the United States (references). Nonetheless, it has been well established that obesity significantly contributes to the pathogenesis of many chronic conditions. Emerging data indicates that the relationship between chronic conditions and sleep disorders are likely mediated by the relationship between sleep disorders and obesity. For example, with respect to insomnia, \citet{Taheri2004} showed that shorter sleep durations were associated with 15% lower lepin levels and 14.9% higher ghrelin levels which were independent of Body Mass Index (BMI). They conclude that chronically shortened sleep duration could increase appetite leading to overeating and eventually obesity. The neuro-cognitive theory of insomnia suggests that insomnia is associated with increased levels of cortisol \citep{Perlis1997}. \citet{Dallman2003}, proposed that chronic evaluation of gluocorticoids, such as cortisol may be implicated in the overconsumption of high fat and sugary foods and the propensity to store fat around the abdominal area. They argue that chronically elevated levels of glucocortical hormones increase corticotropin-releasing factor activity in the central nucleus of the amygdala which increases stimulus salience and abdominal obesity. This mechanism then moderates metabolic inhibitory feedback on the catecholamines in the brain and the expression of corticotropin-releasing factor. Accordingly, the authors propose that, in an attempt to dampen activity in the brain, the same mechanisms which mediates hyperactivity in insomnia facilitates overconsumption of high fat and sugary foods as well as promoting abdominal obesity. Population studies have also demonstrated a strong associated between OSA and chronic diseases including cardiovascular disease, hypertension, diabetes mellitus and stroke (Somer et al, 2008) \citep{Kato2009}. Moreover, as with insomnia, a strong relationship has also been shown between OSA and obesity and emerging evidence suggests a reciprocal interaction \citep{Passos2010}. \citep{Malhotra2002}. \citet{Ong2013} propose that obesity causes changes to the upper airway structure and function, causes 'reductions in resting load volume and negative effects on respiratory drive and load compensation' compensation' \citep{Hargens_2013}.