The relationship between chronic sleep restriction, poor sleep quality and obesity in adults

This thesis consists of two literature reviews followed by three empirical chapters that examined the relationship between chronic sleep restriction and obesity. Chapter 2 reviewed available research data and presented a theoretical model linking chronic sleep restriction to obesity. This model hypothesises that chronic sleep restriction contributes to obesity by altering energy regulatory hormones such as ghrelin and leptin. It was also argued that factors such as poor mental health, medication use and long work hours contribute to chronic sleep restriction at a population level, and could have implications for improving sleep. This model provides a sound theoretical framework, which was used to guide the subsequent empirical chapters. In chapter 3, the key methodological limitations of previous studies examining the relationship between chronic sleep restriction and obesity were outlined. Methodological recommendations for future research were then provided to facilitate a more complete understanding of how chronic sleep restriction and obesity are linked in the general population. Chapter 4 tested a path model linking chronic sleep restriction to obesity in 325 adults aged 18 to 87 years, based on the theoretical framework provided in chapter 2 and the methodological recommendations listed in chapter 3. The results indicated that short sleep durations and age were associated with obesity, whilst age, uncomfortable sleep environments, irregular sleep/wake cycles and poor mental health were associated with short sleep durations. However, the results also identified potential environmental, behavioural and psychological determinants of chronic sleep restriction that could be targeted in the future treatment and prevention of obesity. Chapter 5 examined the relationship between three dimensions of sleep quality as assessed by the Pittsburgh Sleep Quality Index and obesity in 262 adults aged 18 to 35 years. Short sleep durations and increased levels of daytime dysfunction (e.g., sleepiness) were associated with obesity, whilst irregular bedtimes, noisy environments, discomfort and depression were the major factors associated with poor sleep quality. These factors could play a role in obesity interventions that target sleeping patterns and need to be further investigated. Finally, chapter 6 examined the effects of two nights of seep restriction on energy expenditure and neuroendocrine hormones involved in energy balance regulation in ten healthy male adults. The results indicated that sleep restriction led to an increase in ghrelin and a reduction in PYY, which corresponded with increased hunger and reduced satiety. The results also suggested that energy expenditure declined with sleep restriction. These results suggest that sleep restriction could contribute to obesity by altering energy expenditure and the hormonal regulation of food intake. The findings from this thesis therefore suggest that chronic sleep restriction contributes to the development of obesity by altering key pathways identified in chapter 2. The identification of possible determinants of chronic sleep restriction has potential applications for the treatment and prevention of obesity. For example, the factors identified in chapters 4 and 5 could be targeted as a way to promote healthy sleep durations, and could be effective in improving the efficacy of existing interventions for obesity