Does inadequate sleep play a role in vulnerability to obesity?

Section of Pulmonary/Critical Care, Department of Medicine, University of Chicago, Illinois 60622, USA.
American Journal of Human Biology (Impact Factor: 1.7). 05/2012; 24(3):361-71. DOI: 10.1002/ajhb.22219
Source: PubMed

ABSTRACT The prevalence of obesity is increasing rapidly worldwide, which is cause for concern because obesity increases the risk of cardiovascular disease and diabetes, reduces life expectancy, and impairs quality of life. A better understanding of the risk factors for obesity is therefore a critical global health concern, and human biologists can play an important role in identifying these risk factors in various populations. The objective of this review is to present the evidence that inadequate sleep may be a novel risk factor associated with increased vulnerability to obesity and associated cardiometabolic disease. Experimental studies have found that short-term sleep restriction is associated with impaired glucose metabolism, dysregulation of appetite, and increased blood pressure. Observational studies have observed cross-sectional associations between short sleep duration (generally <6 h per night) and increased body mass index or obesity, prevalent diabetes, and prevalent hypertension. Some studies also reported an association between self-reported long sleep duration (generally >8 h per night) and cardiometabolic disease. A few prospective studies have found a significant increased risk of weight gain, incident diabetes, and incident hypertension associated with inadequate sleep. Given the potential link between inadequate sleep and obesity, a critical next step is to identify the social, cultural, and environmental determinants of sleep, which would help to identify vulnerable populations. Future human biology research should consider variation in sleep characteristics among different populations and determine whether the associations between sleep and obesity observed in Western populations persist elsewhere.

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Available from: Kristen L Knutson, Sep 26, 2015
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    • "Speculatively, short sleep durations may be implicated in the aetiology of obesity. Supporting this theory, laboratory studies in adults have shown that restricted sleep deregulates endocrine secretions , causing decreased leptin and increased ghrelin, which may predispose to obesity through increased energy intake [12]. Physical activity, sedentary time, and depression have also been proposed as mediating factors [13]. "
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    ABSTRACT: The objective of this study was to investigate whether objectively measured sedentary time and sleep duration are associated with changes in adiposity from mid- to late adolescence. Students (n = 504, 42% boys) were recruited from schools in Cambridgeshire, UK. At baseline (mean age 15.0 ± 0.3 years), sedentary time was objectively measured by ≥3 days of combined heart rate and movement sensing. Concurrently, sleep duration was measured by combined sensing in conjunction with self-reported bed times. Fat mass index (FMI; kg/m(2)) was estimated at baseline and follow-up (17.5 ± 0.3 years) by anthropometry and bioelectrical impedance. FMI change (ΔFMI) was calculated by subtracting the baseline from follow-up values. Linear regression models adjusted for basic demographics, moderate-to-vigorous physical activity (MVPA), and depressive symptoms were used to investigate associations of sedentary time and sleep duration (mutually adjusted for one another) with ΔFMI. FMI increased by 0.5 and 0.6 kg/m(2) in boys and girls, respectively, but there was no association between sedentary time and ΔFMI in either gender (p ≥ 0.087), and no association between sleep duration and ΔFMI in girls (p ≥ 0.61). In boys, each additional hour of baseline sleep significantly reduced the ΔFMI by 0.13 kg/m(2) (p = 0.049), but there was little evidence for this association after adjusting for MVPA and depressive symptoms (p = 0.15). Sedentary time may not determine changes in adiposity from mid- to late adolescence, nor may sleep duration in girls. However, sleep length may be inversely associated with adiposity gain in boys, depending on whether the relationship is confounded or mediated by MVPA and depression. Copyright © 2015 The Authors. Published by Elsevier B.V. All rights reserved.
    Sleep Medicine 03/2015; 16(6). DOI:10.1016/j.sleep.2015.02.532 · 3.15 Impact Factor
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    • "Insomnia symptoms are very common, affecting one-third of the adult population; insomnia disorder is the most prevalent among the sleep disorders afflicting approximately 6–10% of adults [1]. Experimental and epidemiological studies conducted in adults show that poor sleep and insomnia have a wide spectrum of sequelae , including neuroendocrine and cardiovascular alterations as well as psychiatric and neurodegenerative disorders [2] [3] [4] [5] [6] [7] [8] [9]. From a life-course perspective on health, understanding the early-life origins of insomnia may be particularly useful in order to prevent and treat this disturbance, which is of high economic relevance for healthcare systems [10]. "
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    ABSTRACT: Insomnia is very common in the adult population and it includes a wide spectrum of sequelae, that is, neuroendocrine and cardiovascular alterations as well as psychiatric and neurodegenerative disorders. According to the conceptualization of insomnia in the context of the 3-P model, the importance of predisposing, precipitating, and perpetuating factors has been stressed. Predisposing factors are present before insomnia is manifested and they are hypothesized to interact with precipitating factors, such as environmental stressful events, contributing to the onset of insomnia. Understanding the early-life origins of insomnia may be particularly useful in order to prevent and treat this costly phenomenon. Based on recent evidence, prenatal-early-life stress exposure results in a series of responses that involve the stress system in the child and could persist into adulthood. This may encompass an activation of the hypothalamic-pituitary-adrenal axis accompanied by long-lasting modifications in stress reactivity. Furthermore, early-life stress exposure might play an important role in predisposing to a vulnerability to hyperarousal reactions to negative life events in the adult contributing to the development of chronic insomnia. Epigenetic mechanisms may also be involved in the development of maladaptive stress responses in the newborn, ultimately predisposing to develop a variety of (psycho-) pathological states in adult life. Copyright © 2014 Elsevier B.V. All rights reserved.
    Sleep Medicine 01/2015; 16(4). DOI:10.1016/j.sleep.2014.10.013 · 3.15 Impact Factor
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    • "Besides the decreased quality of life that was associated with these sleeping difficulties [4], the clinical relevance and consequences of possible circadian dysregulation in NFMA patients might be further underlined and assessed by an increased risk for cardiovascular disease. Circadian dysregulation due to hypothalamic damage is associated with the metabolic syndrome both directly, a syndrome known as hypothalamic obesity after structural hypothalamic damage [5], and indirectly, through the consequences of decreased sleep duration and quality [6]. In addition, intrinsic imperfections of hormone replacement therapy might increase the risk for the metabolic syndrome in NFMA patients. "
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    ABSTRACT: Patients treated for nonfunctioning pituitary macroadenoma (NFMA) with suprasellar extension show disturbed sleep characteristics, possibly related to hypothalamic dysfunction. In addition to hypopituitarism, both structural hypothalamic damage and sleep restriction per se are associated with the metabolic syndrome. However, the prevalence of the metabolic syndrome in patients with NFMA is not well established. Our objective was to study the prevalence and risk factors for (components of) the metabolic syndrome in patients treated for NFMA. The metabolic syndrome (NCEP-ATP III criteria) was studied in an unselected cohort of 145 NFMA patients (aged 26-88yr, 44% female) in long-term remission after treatment, receiving adequate stable hormone replacement for any pituitary deficiencies. The results were compared to population data of 63,995 Dutch inhabitants by standardization (LifeLines cohort study). NFMA patients showed increased risk for reduced HDL-cholesterol (SMR 1.59, 95% CI 1.13-2.11), increased triglyceride levels (SMR 2.31, 95% CI 1.78-2.90) and the metabolic syndrome (SMR 1.60, 95% CI 1.22-2.02), but not for increased blood pressure, waist circumference or hyperglycemia. Preoperative visual field defects independently affected the risk for increased blood pressure (OR 6.5, 95% CI 1.9-22.2), and hypopituitarism was associated with a body mass index - dependent risk for increased waist circumference (OR 1.6, 95% CI 1.2-2.2) and the metabolic syndrome (OR 1.4, 95% CI 1.0-1.9). Patients treated for NFMA are increased at risk for developing the metabolic syndrome, mainly due to decreased HDL-cholesterol and increased triglycerides. Risk factors included hypopituitarism and preoperative visual field defects. Hypothalamic dysfunction may explain the metabolic abnormalities, in addition to intrinsic imperfections of hormone replacement therapy. Additional research is required to explore the relation between derangements in circadian rhythmicity and metabolic syndrome in these patients.
    PLoS ONE 03/2014; 9(3):e90602. DOI:10.1371/journal.pone.0090602 · 3.23 Impact Factor
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