Which of the following sleep disorders is most strongly associated with obesity?

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Poor sleep quality, which is often associated with overall sleep loss, has also become a frequent complaint. Do you know which of the following sleep disorders is most strongly associated with obesity?

Growing evidence both from laboratory and epidemiological studies points to short sleep duration as a new risk factor for the development of obesity and its complications. Sleep is an important modulator of neuroendocrine function and glucose metabolism and sleep loss has been shown to result in metabolic and endocrine alterations, including decreased glucose tolerance and alteration of appetite regulating hormone.

To short sleep duration as a new risk factor for the development of obesity

To short sleep duration as a new risk factor for the development of obesity

Insomnia and obesity

Previous studies have indicated that persons with obesity are significantly more likely to report insomnia or difficulty with sleep.19 Additionally, over an average 7.5-year follow-up, persons with obesity were significantly more likely to develop chronic insomnia, although this effect was partially negated when controlling for sociodemographic and behavioral factors. Finally, in persons with obesity, complaints of chronic emotional stress or sleep disturbance have been reported to be predictors for short sleep duration, rather than voluntary sleep curtailment as previously thought. Vgontzas et al further showed that in persons with obesity and without sleep disturbances or emotional stress, sleep duration was similar to non-obese control subjects. This may indicate the importance of detection and treatment of sleep disturbances as a potential therapeutic intervention for obesity.

Insomnia, or its underlying pathophysiology, may play a role in predisposing one to overconsumption of energy, thus leading to weight gain. In a study of over 1000 volunteers from the Wisconsin Sleep Cohort Study, Taheri et al found that shorter sleep durations (5 hours per night versus 8 hours per night) were associated with 15.5% lower leptin levels and 14.9% higher ghrelin levels, independent of BMI, which may indicate that chronically shortened sleep duration could increase appetite, leading to overconsumption. Additionally, Dallman et al have proposed that chronic elevation of glucocorticoids, such as cortisol, similar to the proposed mechanism for insomnia, may play a role in increasing a person’s desire to consume high fat and high sugar foods, as well as their propensity to store fat in the abdominal region. They proposed that the chronically elevated levels of glucocorticoid hormones increase CRF activity in the central nucleus of the amygdala, increase stimulus salience, and increase abdominal obesity, which then serves as a means of increasing the metabolic inhibitory feedback on the catecholamines in the brain and CRF expression. This would indicate that the same pathway associated with hyperactivity in insomnia may promote the overconsumption of high fat and high sugar foods, as well as the deposition of abdominal fat stores, in an attempt to calm the hyperactivity occurring in the brain

Insomnia may promote the overconsumption of high fat and high sugar foods

Sleep duration and obesity risk: epidemological evidence

Sleep ‘is a restorative process of the brain, by the brain, and for the brain’, but it is now clear that sleep is important for health of the entire body. The decrease in sleep duration and increase in sleep complaints in modern society raise concerns for a negative impact of chronic sleep disturbances on health in general, not only mental health.

Behavioral sleep curtailment is becoming endemic in modern times. Ours is a 24-h society with more evening and night-time work and leisure activities, which all lead to a sacrifice of hours available for sleep. This has had a major impact on sleep time, duration of dark exposure, and overall organization of circadian rhythms through the exposure to artificial light after sunset and often before sunrise, resulting in later bedtimes, reduced total sleep time, and the opportunity to be active and ingest food during the natural night.

Feeding represents a major synchronizer of peripheral circadian clocks, which have been found in virtually all tissues. Delayed feeding due to prolonged night-time wakefulness leads to desynchrony between central circadian and peripheral clocks .


Indeed circadian desynchrony as it occurs in shift workers is associated with cardiometabolic alterations and increased risk of metabolic syndrome and cardiovascular disease . On the basis of the link between circa-dian desynchrony and obesity and metabolic disorders, obesity could represent a ‘chronobiological disease’ .

To date, approximately 50 epidemiological studies done in different geographical regions have examined the association between sleep and obesity in adults and children. The majority found a significant association between short sleep (generally <6 h per night) and increased obesity risk. A meta-analysis of 18 studies in 604 509 adults demonstrated a pooled obesity odds ratio (OR) of 1.55 (1.43–1.68; P < 0.0001) for less than 5 h of sleep and a dose effect of sleep duration such that for each additional hour of sleep BMI decreased by 0.35 kg/m2.

Sleep duration and obesity risk: laboratories studies

The relationship between sleep and obesity is likely mediated by multiple pathways. An upregulation of the activity of orexin neurons and changes in appetite-regulating hormones may affect food intake. It has been previously shown that ghrelin, a hormone promoting hunger, increases with sleep restriction, whereas leptin, a hormone contributing to satiety perception, decreases. More recently, Spiegel et al. analyzed the 24 h ghrelin profile in relation to meal and sleep in 14 healthy young men and showed an inhibitory effect of sleep on ghrelin secretion.

Figure 1 provides a schematic representation of the orexin system, which represents the link between sleep and feeding. Orexigenic neurons regulate the homeostatic feeding center in the hypothalamic arcuate nucleus, and concurrently affect hedonic feeding mediated by the ‘reward centers’ (ventro-tegmental area and nucleus accumbens) . Leptin and ghrelin are peripheral signals directly interacting with the arcuate nucleus, and ultimately modulating the orexin system activity to decrease and increase food intake, respectively. Their secretion is also modulated by the autonomic nervous system activity. A shift of the sympathovagal balance to higher sympathetic activity has been observed in studies of sleep deprivation

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