Sleep and weight loss

 Good sleep is a foundation for good health and a happier frame of mind.

Over the past few decades, both sleep quality and quantity has declined. In fact, 

many people regularly get poor sleep due to stress from work, poor sleeping 

environment, etc. 

Getting a good night’s sleep is one of the most important things you can do for 

health and weight loss. 

Extracted from pubmed.gov

According to the journal "Impact of sleep and sleep loss on neuroendocrine and 

metabolic function"  Sleep exerts important modulatory effects on neuroendocrine 

function and glucose regulation. During the past few decades, sleep curtailment has

 become a very common behavior in industrialized countries. This trend toward 

shorter sleep times has occurred over the same time period as the dramatic 

increases in the prevalence of obesity and diabetes. 

  Laboratory studies in healthy young volunteers have shown that experimental 

sleep restriction is associated with a dysregulation of the neuroendocrine control of

 appetite consistent with increased hunger and with alterations in parameters of 

glucose tolerance suggestive of an increased risk of diabetes. Epidemiologic 

findings in both children and adults are consistent with the laboratory data.

Another study "Sleep disturbances, body fat distribution, food 

intake and/or energy expenditure: pathophysiological aspects" 

found out that  Individuals with SSD/short sleep duration are 

heavier and gain more weight over time than normal-duration 

sleepers. This sleep-obesity relationship may have 

consequences for obesity treatments, as it appears that short 

sleepers have reduced ability to lose weight. Laboratory-based

 clinical studies found that experimental sleep restriction 

affects energy expenditure and intake, possibly providing a 

mechanistic explanation for the weight gain observed in 

chronic short sleepers. Specifically, compared to normal sleep 

duration, sleep restriction increases food intake beyond the 

energetic costs of increased time spent awake. Reasons for 

this increased energy intake after sleep restriction are unclear 

but may include disrupted appetite-regulating hormones, 

altered brain mechanisms involved in the hedonic aspects of 

appetite, and/or changes in sleep quality and architecture. 

Obstructive sleep apnea (OSA) is a disorder at the intersection 

of sleep and obesity, and the characteristics of the disorder 

illustrate many of the effects of sleep disturbances on body 

weight and vice versa. Specifically, while obesity is among the 

main risk factors for OSA, the disorder itself and its associated 

disturbances in sleep quality and architecture seem to alter 

energy balance parameters and may induce further weight 

gain. Several intervention trials have shown that weight loss is 

associated with reduced OSA severity. Thus, weight loss may 

improve sleep, and these improvements may promote further 

weight loss. Future studies should establish whether 

increasing sleep duration/improving sleep quality can induce 

weight loss.

Short sleep duration and obesity are common occurrence in today's society. An 

extensive literature from cross-sectional and longitudinal epidemiological studies 

shows a relationship between short sleep and prevalence of obesity and weight 

gain. However, causality cannot be inferred from such studies. Clinical intervention 

studies have examined whether reducing sleep in normal sleepers, typically 

sleeping 7-9 h/night, can affect energy intake, energy expenditure, and endocrine 

regulators of energy balance. The aim of this review is to evaluate studies that have

 assessed food intake, energy expenditure, and leptin and ghrelin levels after 

periods of restricted and normal sleep. Most studies support the notion that 

restricting sleep increases food intake, but the effects on energy expenditure are 

mixed. Differences in methodology and component of energy expenditure analyzed 

may account for the discrepancies. Studies examining the effects of sleep on leptin

 and ghrelin have provided conflicting results with increased, reduced, or 

unchanged leptin and ghrelin levels after restricted sleep compared to normal 

sleep. Energy balance of study participants and potential sex differences may 

account for the varied results. Studies should strive for constant energy balance 

and feeding schedules when assessing the role of sleep on hormonal profile. 

Although studies suggest that restricting sleep may lead to weight gain via 

increased food intake, research is needed to examine the impact on energy 

expenditure and endocrine controls. Also, studies have been of short duration, and 

there is little knowledge on the reverse question: does increasing sleep duration in 

short sleepers lead to negative energy balance?

Insufficient sleep and poor quality sleep are pervasive during adolescence and 

relate to impairments in cognitive control and increased risk taking. However, the 

neurobiology underlying the association between sleep and adolescent behavior 

remains elusive. In the current study, we examine how poor sleep quality relates to 

cognitive control and reward related brain function during risk taking. Forty-six 

adolescents participated in a functional magnetic imaging (fMRI) scan during which 

they completed a cognitive control and risk taking task. Behaviorally, adolescents 

who reported poorer sleep also exhibited greater risk-taking. This association was 

paralleled by less recruitment of the dorsolateral prefrontal cortex (DLPFC) during 

cognitive control, greater insula activation during reward processing, and reduced 

functional coupling between the DLPFC and affective regions including the insula 

and ventral striatum during reward processing. Collectively, these results suggest 

that poor sleep may exaggerate the normative imbalance between affective and 

cognitive control systems, leading to greater risk-taking in adolescents.

Compared to a few decades ago, adults, as well as children, sleep less. Sleeping 

as little as possible is often seen as an admirable behavior in contemporary society. 

However, sleep plays a major role in neuroendocrine function and glucose 

metabolism. Evidence that the curtailment of sleep duration may have adverse 

health effects has emerged in the past 10 years. Accumulating evidence from both 

epidemiologic studies and well-controlled laboratory studies indicates that chronic 

partial sleep loss may increase the risk of obesity and weight gain. The present 

chapter reviews epidemiologic studies in adults and children and laboratory studies 

in young adults indicating that sleep restriction results in metabolic and endocrine 

alterations, including decreased glucose tolerance, decreased insulin sensitivity, 

increased evening concentrations of cortisol, increased levels of ghrelin, decreased 

levels of leptin and increased hunger and appetite. Altogether, the evidence points 

to a possible role of decreased sleep duration in the current epidemic of obesity. 

Bedtime extension in short sleepers should be explored as a novel behavioral 

intervention that may prevent weight gain or facilitate weight loss. Avoiding sleep

 deprivation may help to prevent the development of obesity, particularly in children.