Relationship between short sleeping hours and childhood overweight/obesity: results from the ‘Québec en Forme’ Project

Chaput, Jean‐Philippe; Brunet, Marie-Christine; Tremblay, Angelo

doi:10.1038/sj.ijo.0803291

Cited by 304 publications

(260 citation statements)

References 24 publications

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“…53 Thus, the dramatic increase in the incidence of obesity and type 2 diabetes seems to have developed over the same period of time as the progressive decrease in self-reported sleep duration. [54][55][56] A growing body of epidemiological evidence supports an association between short sleep duration and the risk of obesity [57][58][59][60][61] and type 2 diabetes. [62][63][64][65][66] The potential mechanisms by which sleep deprivation may predispose to obesity are: (1) an alteration of the neuroendocrine control of appetite characterized by a decrease in the levels of the anorexigenic hormone leptin and an increase in the levels of the orexigenic hormone ghrelin; (2) an increased opportunity to eat; (3) an altered thermoregulation; and (4) an increased fatigue leading to reductions in physical activity.…”

Section: Short Sleep Duration: Association With Glucose Homeostasismentioning

confidence: 99%

The glucostatic theory of appetite control and the risk of obesity and diabetes

Chaput

Tremblay

2008

Int J Obes

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More than 50 years ago, Jean Mayer proposed that changes in blood glucose concentrations or arteriovenous glucose differences are detected by glucoreceptors that affect energy intake. According to this theory, an increase in blood glucose concentrations results in increased feelings of satiety whereas a drop in blood glucose concentrations has the opposite effect. The pioneering work of Mayer has recently received support from our group as low glycemia has been shown to be linked with body weight gain prospectively and has been considered as a strong predictor of the amount of weight regained after weight loss. This state of mild hypoglycemia also predicts the increase in depressive symptoms with weight loss and a greater propensity to glucose intolerance and type 2 diabetes, particularly for individuals having short sleep durations. Furthermore, knowledgebased work has been shown to induce a significant increase in spontaneous energy intake being related to changes in glycemic control. In accordance with the glucostatic theory, this oriented review suggests that factors favoring a trend toward hypoglycemia and/or glucose instability might induce excess energy intake, overweight and impaired glucose tolerance. Data also raise the possibility that fat gain might be protective against mild hypoglycemia by providing compensation to the stimuli promoted by a modern environment. Keywords: body weight; glycemia; glucose homeostasis; glucose intolerance; metabolism; weight gainThe identification of the biochemical basis for hunger and meal initiation, and of the signals controlling these neurobiological processes have been the subject of extensive research and debate for some decades regarding the control of food intake. These studies led to the classical lipostatic, 1 aminostatic, 2 and thermostatic 3 theories of food intake control as well as more recent hypotheses. [4][5][6] However, all of these theoretical ideas were preceded by the notion that glucose uptake and utilization played a central and metabolically privileged role in the control of hunger, satiety and the regulation of body energy balance. Although these notions were first discussed and suggested by Carlson in a classic text published in 1916, 7 they were formalized by Jean Mayer into the classical glucostatic theory in the mid 1950s. 8,9 The glucostatic theory of food intake control postulated that reduced glucose utilization in critical brain regions leads to perception and expression of hunger, and increased glucose utilization in these same glucosensitive sites leads to decreased hunger and cessation of eating. Mayer proposed that decreased glucose utilization or 'metabolic hypoglycemia', the point at which the peripheral arteriovenous difference in blood glucose becomes negligible and glucose is no longer entering 'metabolizing cells', was the signal for meal initiation. In his 1955 paper, Mayer explicitly argued that the glucostatic theory would account for the short-term control of hunger and food intake, whereas he invoked a lipostatic mechanism...

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Section: Short Sleep Duration: Association With Glucose Homeostasismentioning

confidence: 99%

The glucostatic theory of appetite control and the risk of obesity and diabetes

Chaput

Tremblay

2008

Int J Obes

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“…6,7 The most probable sleep factor linked with obesity is sleep duration. Cross-sectional evidence suggests an association between short sleep and obesity in children [8][9][10][11] and in young adults. [12][13][14][15] In addition, two prospective cohort studies have shown that short sleep predicts future weight gain in young adults 16 and in middle-aged women.…”

Section: Introductionmentioning

confidence: 99%

Sleep-related disturbances and physical inactivity are independently associated with obesity in adults

Kronholm²,

et al. 2007

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Objective: To study relationships between obesity, physical inactivity and sleep-related disturbances (obstructive sleep apnea (OSA), sleep duration, sleep disturbances concomitant with daytime tiredness) in adults (X30 years). Design: Cross-sectional study with a random population sample. Participants: A total of 3377 men (mean age 52.3, s.d. 14.8, years) and 4264 women (56.4, s.d. 17.2, years). Main outcome measures: Dependent variables, measured: Waist circumference (WC) and body mass index (BMI). Independent variables, from a detailed interview/questionnaire: probable OSA, other sleep-related disturbances, sleep duration, type and frequency of leisure physical activity. Age, mental health, smoking and education were included in analyses as potential confounders. Results: In men, OSA and physical inactivity increased likelihood for abdominal obesity (WC X102 cm). Physical inactivity also increased, but long (X9 h/day) sleep decreased likelihood for abdominal overweight (WC: 94-101 cm) in men. In women, abdominal obesity (WC X88 cm) was associated positively with OSA, moderate sleep-related disturbances, and physical inactivity. Education modulated the influence of age on abdominal obesity in both genders. Using BMI as the dependent variable did not change the general information obtained by the model. In addition, abdominal obesity was found to be an independent risk factor also in multivariable models predicting categories of a combined sleep duration and sleep disturbances. Conclusions: Sleep duration and sleep-related disturbances are associated with obesity, even after controlling for OSA and physical inactivity. The results support the hypothesis of vicious circle between sleep and obesity.

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“…1 The increase in childhood obesity has developed over the same time period as the progressive decrease in self-reported sleep duration. 2,3 Several crosssectional studies reported on an inverse relationship between body mass index (BMI) and sleep duration during childhood [4][5][6][7][8][9] ; some reported a curvilinear relationship between BMI and sleep duration. 10,11 Additionally, short sleep duration in children was related to insulin resistance, a larger body fat percentage, a larger waist circumference, decreased physical activity and increased television watching.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, the polymorphisms of the FTO gene (rs9939609) and parental BMI's were determined, since they might be potential confounders as has been shown in previous studies. 9,17,[24][25][26][27] Subjects and methods…”

Section: Introductionmentioning

confidence: 99%

Sleep duration and body-weight development during puberty in a Dutch children cohort

et al. 2010

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Background: Short sleep duration is associated with obesity during childhood and adulthood. Objective: The objective of our study was to investigate the relationship between sleep duration and body mass index (BMI) from Tanner stages 1 to 5 in a Dutch children cohort. Design: In 98 children, anthropometric measurements and leptin concentrations were measured from age 7 to 16 years; body composition, physical activity (Baecke questionnaire), hours television viewing and self-reported sleep duration were measured yearly from age 12 to 16 years. Moreover, the polymorphisms of the FTO gene (rs9939609) and parental BMI's were determined. Results: At Tanner stages 1-5 sex differences were observed in height, body weight, waist circumference, fat mass per squared meter height and leptin concentrations per kg fat mass. Inverse relationships were observed between the change in BMI (kg m -2 ) and the change in hours of sleep per night (h) from Tanner stages 1 to 4 (r ¼ À0.68, Po0.001), from Tanner stages 2 to 5 (r ¼ À0.35, Po0.05) and from Tanner stages 1 to 5 (r ¼ À0.33, Po0.05). Univariate analysis of variance showed that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way independent of possible confounders (R 2 ¼ 0.38, Po0.02). Conclusion: Changes in BMI during puberty were inversely related to changes in sleep duration, independent of possible confounders.

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Relationship between short sleeping hours and childhood overweight/obesity: results from the ‘Québec en Forme’ Project

Cited by 304 publications

References 24 publications

The glucostatic theory of appetite control and the risk of obesity and diabetes

The glucostatic theory of appetite control and the risk of obesity and diabetes

Sleep-related disturbances and physical inactivity are independently associated with obesity in adults

Sleep duration and body-weight development during puberty in a Dutch children cohort

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