Overweight and obesity are leading causes of morbidity and mortality in the United States. Prevalence of U.S. youth over the 85th percentile of weight now approaches 33% (Skinner, Ravanbakht, Skelton, Perrin, & Armstrong, 2018). Youth are also frequently affected by sleep deprivation, which occurs in approximately 27% of school-aged children and 45% of adolescents (Buxton et al., 2015). Contributing factors of sleep deprivation in youth may include timing of meals, caffeine consumption, increased use of electronics, and decreased physical activity.
Adequate sleep is necessary for cognitive functioning, memory, and mood stabilization. Conversely, insufficient sleep can affect verbal fluency, temporal memory, logical memory, planning, and decision making (Muzur, Pace-Schott, & Hobson, 2002). Sleep is driven by a physiological need similar to hunger and is quantified by time to sleep onset, arousal threshold to sleep, and duration of sleep. Sleep is modulated by environment, motivation, and external and internal stimulation. The drive for sleep can be overruled by voluntary sleep restriction; it may be interrupted by environmental factors or disorders such as obstructive sleep apnea (OSA), insomnia, restless leg syndrome, or narcolepsy (Nedeltcheva & Scheer, 2014).
The National Sleep Foundation recommends that newborns between 0 and 3 months old sleep 14–17 hours per day; infants, 12–15 hours per day; toddlers, 11–14 hours per day; preschoolers, 10–13 hours per day; and school-aged children, 9–11 hours per day. Teenagers need 8–10 hours of sleep per day (Hirshkowitz et al., 2015). Insufficient sleep leads to fatigue, excessive daytime sleepiness, lower quality of life, reduced cognitive and motor performance, and an increased risk of memory disorders long term (Beebe, 2016).
Sleep fragmentation such as OSA disrupts sleep architecture. OSA is a partial to complete upper airway obstruction that occurs more than five times in an hour (apnea–hypopnea index). OSA with excessive daytime sleepiness, known as OSA syndrome, is an independent risk factor for cardiovascular disease and metabolic disorders and is linked to systemic hypertension, coronary disease, abnormal glucose metabolism, and stroke (Andersen, Holm, & Homøe, 2016).
Animal models suggest OSA contributes to adipocyte dysfunction. Apneics tend to have increased fat within the tongue, independent of body mass index (BMI), age, gender, and race (Kim et al., 2014). In children, OSA is linked to craniofacial syndromes, choanal stenosis, subglottic stenosis, Down syndrome, and Prader–Willi syndrome (Hakim, Kheirandish-Gozal, & Gozal, 2015).
ASSOCIATION BETWEEN SLEEP DISRUPTION AND OBESITY
Sleep impacts hormones within the body's endocrine system. In normal sleep, growth hormone secretion slows during the normal sleep cycle. Cortisol also follows this circadian rhythm, drops with slow wave sleep, and increases with wakening. Sleep quality and quantity affect insulin secretion and glucose regulation (Reutrakul & Van Cauter, 2018).
Sleep disruption may negatively impact two energy hormones, leptin and ghrelin, which control appetite. Leptin, secreted by adipose tissue in response to satiety, peaks between 10:00 p.m. and 03:00 a.m. during sleep. However, leptin is markedly decreased after sleep deprivation. Ghrelin, the “hunger” hormone, is secreted in the fundus of the stomach. Ghrelin is lowest during sleep, peaks before meals, and decreases after a meal. Lack of sleep increases ghrelin, which may lead to increased food ingestion. Ghrelin is linked to glucose intolerance and insulin resistance (Deng et al., 2017).
Short sleep duration appears to increase risk of obesity in children and adolescents. Fatima, Doi, and Mamun (2015) performed a systematic review and meta-analysis focusing on possible links between sleep problems in children and adolescents and overweight/obesity. The results suggest that sleep deprivation is inversely associated with subsequent elevated BMI percentiles in children and adolescents. Those who sleep for shorter periods have twice the odds of overweight and obesity compared with those who sleep for longer durations.
Adolescents with sleep disturbances are at a higher risk of overweight and obesity compared with younger children, perhaps partially explained by the combination of short sleep duration and biological and lifestyle-related changes associated with adolescence (Owens, 2014 ; Owens & Weiss, 2017). Sleep curtailment may also lead to daytime sleepiness with reductions in physical activity and energy metabolism. Short duration of sleep may facilitate energy intake and decrease energy expenditure by affecting hormones secreted from adipocytes, which act on receptors in the hypothalamus. Although obesity is a multifactorial problem, mostly controlled by our genetic makeup and hormones, behavioral interventions aimed at improving sleep duration may help reduce overweight and obesity.
SCREENING FOR SLEEP DISTURBANCES
Screening for sleep disturbances is an essential component within a history and physical examination. A complete sleep history, including sleep patterns and areas of concern, will guide the treatment plan. Several screening tools are used with children and adolescents (Shahid, Shen, & Shapiro, 2010 ; Shahid, Wilkinson, Marcu, & Shapiro, 2011). The BEARS sleep screening tool evaluates sleep categories related to Bedtime problems, Excessive daytime sleepiness, Awakenings during the night, Regularity and duration of sleep, and Sleep-disordered breathing (Mindell & Owens, 2015). Questions are available for preschool, school-aged, and adolescent groups. Adult tools, such as the Epworth Sleepiness Scale and STOP-Bang Sleep Apnea questionnaire, have been modified for older adolescents (Shahid et al., 2011). A thorough family, medical, cultural, and psychosocial history along with behavioral assessment and physical examination will guide the need for further testing, treatment, and education.
TREATMENT OF SLEEP DISTURBANCES
Treatment of sleep disturbances is aimed at improving sleep hygiene. Basic principles to improve overall sleep include establishing a bedtime routine, maintaining a consistent sleep schedule, and avoiding caffeine, stimulants, and excessive fluids and food before bedtime as well as optimizing the sleep environment by darkening the bedroom, minimizing ambient light, limiting screen time, and avoiding medications that could interfere with sleep such as benzodiazepines or antihistamines (Halal & Nunes, 2014).
The use of melatonin may be additive to behavioral interventions. Melatonin is secreted in the pineal gland in a rhythmic manner, with high levels during nighttime and low levels during daytime (Golombek, Pandi-Perumal, Brown, & Cardinali, 2015). Melatonin may be effective in restoring the normal onset and offset of sleep–wake phases and may be used for a variety of sleep disruptions. Melatonin is a molecule found in plants and has been synthesized as a medication specifically for the treatment of sleep disruptions.
Treatment of OSA may include tonsillectomy and adenoidectomy, positive airway pressure support, supplemental oxygen, and pharmacological support. Patients with increased weight may benefit from weight loss (Marcus et al., 2012).
Little is known regarding the effect on body composition when eating at a later circadian time. McHill et al. (2017) described a study using food diary results to discover that timing of caloric consumption relative to the onset of melatonin is associated with an increased body fat percentage. Eating after midnight in humans is associated with a higher BMI, and restricting eating to typical waking hours may decrease weight. Meal timing may decrease the thermic effect of food, which is the energy expended in response to a meal. One possible consequence of eating closer to dim light melatonin onset may be a lower thermic effect of food response, which leads to a positive energy balance and weight gain over time (Allison & Tarves, 2011).
Delahaye et al. (2018) conducted a study with mice, showing the greatest benefits when eating within the circadian cycle. Those eating within the circadian cycle gained less weight and maintained better insulin sensitivity than late eaters. Time-restricted feedings also affect the gut microbiome. Microbiota is dynamic and linked to metabolism, immune function, obesity, and other diseases. Time-restricted feedings restored the flora cycle and may protect against metabolic diseases found in mice.
Another intervention aimed at reducing obesity described by Vaughan and Mattison (2018) is intermittent fasting or “time-restricted feeding.” The aim of this intervention is to restrict meal timing to intermittent periods of feeding along with periods of fasting, lasting 6–8 hours, to coincide with sleep combining daily fasting with meals in a normal circadian and metabolic rhythm. This causes the body to shift to alternative metabolic phases using less glucose and more ketone sources. Many benefits are often sustained after the diet regimen has stopped. Timing of most calories coinciding with the time the endocrine system is most responsive may allow more effective processing of meals. There is evidence that benefits from time-restricted feeding may not be only for weight loss. There can also be a decrease in blood pressure, oxidative stress, and insulin with improved insulin sensitivity.
Although the underlying association between sleep and obesity is not fully understood, several potential mechanisms exist, linking reduced sleep and the risk of obesity. Our circadian clock plays an important role in metabolic homeostasis. Sleep disruption can be associated with obesity and other related diseases. Interventions aimed at improving sleep may reduce obesity. Newer research on meal timing relative to melatonin release, intermittent fasting, and the gut microbiome are an emerging new body of evidence, which can be useful tools for practitioners caring for individuals with obesity.
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