Short sleep duration is associated with obesity during childhood and adulthood.
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.
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.
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=−0.68, P<0.001), from Tanner stages 2 to 5 (r=−0.35, P<0.05) and from Tanner stages 1 to 5 (r=−0.33, P<0.05). Univariate analysis of variance showed that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way independent of possible confounders (R2=0.38, P<0.02).
Changes in BMI during puberty were inversely related to changes in sleep duration, independent of possible confounders.
The prevalence of childhood obesity is emerging as a major health problem.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 cross-sectional studies reported on an inverse relationship between body mass index (BMI) and sleep duration during childhood4, 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.12, 13, 14, 15, 16
Longitudinal studies have shown that when young children (prepubertally, up to age 12 years) sleep fewer hours per night, they are at a higher risk to become overweight at a later age, during childhood as well as adulthood.17, 18, 19, 20, 21 Sleep duration during childhood, however, naturally decreases, in particular during puberty when a reduction of about 2 h is observed.22, 23 The relationship between sleep duration and body weight (BW) described in previous longitudinal studies, however, did not take pubertal stages into account, which might influence this relationship. Furthermore, none of the previous studies investigated whether changes in sleep duration are associated with changes in BMI.
Therefore, the objective of our study was to investigate the relationship between BMI and sleep duration longitudinally from Tanner stages 1 to 5. In a Dutch cohort of 98 children, anthropometric measurements and leptin concentrations were measured from age 7 to 16 years; body composition, physical activity (Baecke questionnaire) 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, since they might be potential confounders as has been shown in previous studies.9, 17, 24, 25, 26, 27
Subjects and methods
Subjects were recruited from a Dutch cohort of Caucasian children born between 1990 and 1993. As infants, these children and their mothers—who were randomly selected—participated in (i) a study of essential fatty acids during pregnancy and pregnancy outcome,28 and (ii) a study, performed between 1997 and 2000, about the long-term effects of fetal essential fatty acid availability.29 Anthropometric data were available from these children, no interventions were executed, and follow-up studies were performed with 98 children.25 Exclusion criteria for follow-up measurements were chronic illness and depression, as assessed by medical history. Each child and his or her parents gave written informed consent to participate in the study, which was approved by the Central Committee Human Research and by the medical ethical committee of the Maastricht University.
Every year the follow-up measurements were performed in the months November and December to exclude seasonal effects. At 1600 hours after a 3-h fast children's BW, height, BMI, waist circumference, and leptin concentrations were measured at ages 7–16 years, body composition, physical activity, and self-reported sleep duration were measured at age 12–16 years. Moreover, the polymorphisms of the FTO gene (rs9939609), as well as parental BMI's when the children were 16 years, were determined.
The children's BW was measured using a digital balance accurate to 0.1 kg (Sauter D7470, Ebingen, Germany) and height was measured using a wall-mounted stadiometer (Seca, model 220, Hamburg, Germany). For the measurements the children were wearing underwear. They had fasted for 3 h and had voided the bladder. BMI was calculated by BW per height2 (kg m–2). As BMI in childhood changes substantially with age, we used the specific cutoff points described by Cole et al.30 to define normal weight, overweight and obesity in these children. The waist circumference was measured at the site of the smallest circumference between the rib cage and the ileac crest, with the subjects in standing position. The pubertal stage was documented in all children according to the classification by Tanner, by the two investigators involved in data collection. The Tanner stage is defined and based on physical measurements of external primary and secondary sex characteristics, namely development of breast and pubic hair in girls or development of genitalia and pubic hair in boys. To support Tanner stage definition in the children, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) concentrations were determined. We showed that boys with Tanner stage 1 had LH and FSH levels of 1.7±1.4 and 2.9±2.3 IU l–1 and boys with Tanner stage 5 had LH and FSH levels of 5.7±2.8 and 3.3±1.7 IU l–1. Furthermore, we showed that girls with Tanner stage 1 had LH and FSH levels of 3.0±2.9 and 3.8±2.1 IU l–1 and girls with Tanner stage 5 had LH and FSH levels of 4.4±4.6 and 5.0±4.4 IU l–1. Plasma LH and FSH measurements thus supported Tanner stage definition. Anthropometric measurements were measured at age 7, 12, 13, 14, 15 and 16 years.
Both the parents reported actual BW measured at home according to our standard instructions (as previously described).25 Height was copied from their passports, originally measured using a wall-mounted stadiometer. BMI was calculated by BW per height2 (kg m–2).
Body composition was measured using the deuterium dilution technique (D2O). D2O dilution was used to measure total body water. Subjects were asked to collect a urine sample in the evening just before drinking the deuterium-enriched water solution. After ingestion of this solution, no further consumption was allowed. In the morning the first urine sample was discarded, the whole second urine sample (about 10 h after drinking the water solution) was collected. The dilution of the deuterium isotope is a measure of the total body water of the subject. Deuterium was measured in the urine samples with an isotope ratio mass spectrometer (VG-Isogas Aqua Sira, VG Isogas, Middlewich, Cheshire, UK). Total body water was obtained by dividing the measured deuterium dilution space by 1.04. Fat-free mass was calculated by dividing total body water by the hydration factor 0.73 as defined by Fomon et al.31 Fat mass (FM) was measured as BW–fat-free mass. Fat mass index (FMI) was calculated by fat mass per height2 (kg m–2) and fat-free mass index was calculated by fat-free mass per height2 (kg m–2).32, 33, 34 Body composition was measured at age 12, 13, 14, 15 and 16 years.
At 1600 hours after a 3-h fast, a blood sample was drawn from an intravenous catheter in the forearm vein. Blood was collected and mixed in EDTA tubes (BD Vacutainer, 10 ml, Becton, Dickinson and Company, Erembodegem-Aalst, Belgium). Plasma was obtained by centrifugation (4 °C, 3000 r.p.m., 10 min), frozen in liquid nitrogen and stored at −80 °C. Plasma leptin concentrations were measured with a double-antibody, sandwich-type enzyme-linked immunosorbent assay that used a monoclonal antibody specific for human leptin. The lower limit of detection is 0.5 μg l–1 and the upper limit is 50 μg l–1. The intra- and interassay coefficients of variations were 9 and 12%, respectively. The leptin concentrations of normal-weight subjects ranged from 2 to 12 μg l–1. Plasma leptin concentrations were measured at age 7, 12, 13, 14, 15 and 16 years.
Determination of FTO genotypes
The genomic DNAs of 168 participants were isolated from peripheral blood leukocytes using a QIAamp kit (QIAgen GmbH, Hilden, Germany). FTO (rs9939609) genotypes were determined using Taqman allelic discrimination (AB, Applied Biosystems, Carlsbad, CA, USA). The FTO (rs9939609) genotype was determined because SNP association studies have linked the A allele of this FTO gene to a number of obesity-related characteristics such as increased BMI.35 Furthermore, this genotype was determined because the sample of our cohorts is rather small, and the minor allele frequency of this genotype is over 30%,36 which will give sufficient power to study differences in physiological parameters. This reassured us that the use of the FTO genotype in this smaller cohort was a valid approach.
Physical activity and hours watching television
Physical activity was measured with the Baecke questionnaire.37 Responses to 19 questions were scored on a five-point scale and resulted in three scores: work activity score, sports activity score and leisure activity score. The Baecke questionnaire has been validated using doubly labeled water.38 For the children, the work index was replaced by a school index with similar questions (for example, ‘When I am at school, I walk: never/seldom/sometimes/often/all the time?’). The Baecke questionnaire for children was validated by Vogels et al.26
Hours watching television was measured using the question ‘how many hours do you watch television (TV) per day?’ Physical activity and hours watching television were determined at age 12, 13, 14, 15 and 16 years.
Self-reported sleep duration was measured using the question: ‘how many hours do you sleep per night during weekdays?’, which the children themselves answered and which is supposed to represent their habitual sleep duration.39, 40 Sleep duration was measured at age 12, 13, 14, 15 and 16 years.
Differences between boys and girls per Tanner stage were measured using unpaired t-tests. As hours of sleep per night were measured at age 12–16 years, and not all children were at Tanner stage 1 at age 12 years or Tanner stage 5 at age 16 years, three groups appeared, namely one with data from Tanner stages 1 to 4 (17 males/7 females), one with data from Tanner stages 2 to 5 (24 males/18 females) and one with data from Tanner stages 1 to 5 (14 males/18 females). Univariate analysis of variance was used to assess the relationship between the changes in BMI and changes in sleep duration during the progressive Tanner stages, as well as potential confounders indicated in previous studies,9, 17, 24, 25, 26, 27 such as baseline BMI at start of puberty, FTO allele genotypes, BMI of the father and mother, as well as changes during the progressive Tanner stages in Baecke scores and hours television viewing. Statistical analyses were performed with Statview SE Graphics for Macintosh (Cary, NC, USA). All tests were two-sided and differences were considered significant at P<0.05. Values are expressed as mean±s.d.
Data from 54 boys and 44 girls on height, BW, BMI, waist circumference and leptin concentrations per kg fat mass were collected from age 7 to 16 years, and FMI, Baecke sport score and self-reported hours sleep per night were collected from age 12 to 16 years. The characteristics of the boys and girls from Tanner stages 1 to 5 are represented in Table 1. At Tanner stages 1–5 sex differences were observed in height, BW, waist circumference, FMI and leptin concentrations per kg fat mass. No differences were found in BMI, Baecke sport score and hours sleep per night between boys and girls. From Tanner stages 1 to 5, an increase was observed in both boys and girls in height (0.25±0.15 m, P<0.001 and 0.25±0.15 m, P<0.001), BW (24±12.5 kg, P<0.001 and 26.4±12.5 kg, P<0.001), BMI (3.5±2.7 kg m–2, P<0.001 and 4.9±3.1 kg m–2, P<0.001) and waist circumference (7.6±11.5 cm, P<0.001 and 11.6±7.7 cm, P<0.001), respectively. In the girls also an increase over time in FMI (1.8±2.3 kg m–2, P<0.001) was observed. In boys and girls a decrease was observed in hours sleep per night (−1.2±0.4 h, P<0.001 and −1.4±0.5 h, P<0.001) and in leptin concentrations per kg fat mass (−0.33±0.15 ng ml–1 kg–1, P<0.01 and −0.17±0.2 ng ml–1 kg–1, P<0.01) from Tanner stages 1 to 5. No alterations over time were observed in FMI and Baecke sport scores in boys, while in girls no alterations were observed in Baecke sport scores.
Since hours of sleep per night were measured at age 12–16 years, and not all children were at Tanner stage 1 at age 12 years or Tanner stage 5 at age 16 years, three groups appeared, namely one with data from Tanner stages 1 to 4 (17 males/7 females), one with data from Tanner stages 2 to 5 (24 males/18 females) and one with data from Tanner stages 1 to 5 (14 males/18 females). In all three groups we tested whether changes in BMI over time were related to changes in hours of sleep per night over time. 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=−0.68, P<0.001), from Tanner stages 2 to 5 (r=−0.35, P<0.05) and from Tanner stages 1 to 5 (r=−0.33, P<0.05). Table 2 shows the univariate analysis of variance that assessed the relationship between the changes in BMI (kg m–2) and changes in sleep duration during the progressive Tanner stages, and corrected for possible confounders such as baseline BMI at start of puberty, FTO allele genotype (rs9939609), BMI of the father and mother, as well as changes during the progressive Tanner stages in Baecke scores and hours television viewing. We showed that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way independent of possible confounders (R2=0.38, P<0.02).
The objective of our study was to investigate the relationship between BMI and self-reported sleep duration longitudinally from Tanner stages 1 to 5. We observed sex differences from Tanner stage 1 onward in height, BW, waist circumference, body composition and leptin concentrations per kg fat mass. This was in agreement with previous literature on developmental changes in anthropometry and leptin concentrations normalized to fat mass during puberty.41, 42
We observed a significant reduction in sleep duration during puberty, which is in agreement with previous studies on sleep duration.22, 23 Additionally, we observed an inverse association between pubertal status and sleep duration, which is also in concordance with previous findings.23 These results illustrate the importance of correcting for pubertal stage and not for age for longitudinal and cross-sectional studies on the relationship between BMI and sleep duration, however, age cannot be excluded as an effect modifier of the relationship between BMI and sleep duration.
Earlier longitudinal studies on the relationship between sleep duration and BMI in children observed a consistent association between short habitual sleep duration and later overweight and obesity.17, 18, 19, 20, 21 However, none of these studies investigated whether changes in BMI are associated with changes in sleep duration or studied this relationship during the crucial period of puberty in which sleep duration diverges. We showed, using univariate analysis of variance, that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way, independent of the baseline BMI at start of puberty, FTO allele genotype (rs9939609), BMI of the father and mother, as well as changes during the progressive Tanner stages in Baecke scores and hours television viewing (R2=0.38, P<0.02). Therefore, our study is the first to show that with progressive Tanner stages, BMI increases and sleep duration decreases in an interrelated way independent of possible confounders. From this observed relationship cause and effect cannot be disentangled. A larger increase in BMI following a larger reduction in sleep duration might be plausible, based on the longitudinal study from Snell et al.18 that showed a relationship between sleep duration measured at the first time point and BMI measured after a 5-year interval, and not vice versa. On the other hand, if sleep duration were to be reduced following an increase in BMI, a plausible theory would be sleep apnea. Sleep apnea, however, is only present in 1–3% of the children in a normal population and strongly related to obesity,43 and is therefore an unlikely explanation in our cohort as only 11% of the children were overweight but not obese and with no known cases of sleep apnea.
So, our study might not indicate a mechanism for the association between BMI and sleep duration, but it is important to note that the association was independent of a number of lifestyle factors, such as television viewing and physical activity. The association was also independent of the genetic factor FTO, as well as parental BMI's, which were included to assess both genetic and behavioral associations as well. The association also was independent of BMI at the start of puberty, which moreover suggests that the association is unlikely to be attributable to reverse causation. In other words, it is unlikely that children slept less because they were already overweight.
Several mechanisms can be suggested to explain the relationship between the changes in BMI and in sleep duration during puberty. Puberty is a period of rapid physical, emotional and social maturation44 and it is initiated through pulsatile GnRH release from the hypothalamus and activation of the gonadal axis.45, 46, 47 As a result, secondary sex characteristics develop, including an increase in height44 and behavioral changes, such as a decrease in sleep duration.23 The secondary sex characteristics all originate from shared neuronal systems, with the hypothalamus as integration point.48, 49 The hypothalamus contains the sleep–wake and feeding circuits,48, 49 which are connected through the hypocretin-1 hormone that regulates feeding and locomoter activity via the nucleus accumbens, as well as signals information on the light–dark cycle to the suprachiasmatic nucleus. A lack of hypocretin-1, as seen in children with narcolepsy leads to obesity and precocious puberty.50 This suggests that changes in hypothalamic functioning, such as disturbed hypocretin-1 signaling, might lead to disturbance of the circadian cycle and feeding behavior, affecting energy balance and body composition over time.48, 49 The possibility that disturbed hypothalamic functioning may explain the relationship between the changes in BMI and in sleep duration during puberty is underscored by altered hormone concentrations. For instance, children with short sleep duration show decreases in leptin concentrations, decreased insulin sensitivity and altered cortisol concentrations, all promoting lipogenesis.15, 51, 52 Thus, changes in hypothalamic functioning, such as altered hypocretin-1 signaling may explain the relationship between the changes in BMI and in sleep duration during puberty, via altered puberty onset, energy balance regulation and circadian rhythm. As food-entrainment in addition to light-entrainment, functions as a ‘Zeitgeber’ of the circadian rhythm, possibly alterations in dietary patterns may also explain the relationship between BMI and sleep duration.53 Unfortunately, no information on dietary patterns is available in our study because of unreliability of reported intake in daily life in food intake dairies in children.54 Studies investigating the mechanisms on how sleep duration affects BW development or vice versa in humans are limited. For future research, it is necessary to identify the mechanisms behind the relationship between sleep duration and BW.
Possible limitations of our study are sleep duration being determined using a questionnaire on self-reported sleep duration during weekdays. It would have been more accurate to measure sleep duration using an actigraph or EEG registration, and to also measure sleep duration during weekend days. Previous studies, however, have shown that self-reported sleep duration is representative for habitual sleep duration.39, 40
The strengths of our study are data being collected yearly throughout puberty from a relatively large, general-population, birth cohort, with a high rate of participation, strong tracking of BMI24, 25 and in which no interventions took place. Study members’ heights and weights were measured directly, to provide objective assessments of BMI at all ages. We also were able to control for important covariates that signal a predisposition to increased BMI, including BMI at the start of puberty, polymorphisms of the FTO gene and parental BMI's. Finally, because we assessed sleep times at all stages of puberty, our data are able to show a direct relationship between the changes in BMI and in sleep duration.
Changes in BMI during puberty were inversely related to changes in sleep duration, independent of possible confounders.
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We thank our subjects for their participation in our cohort study. We gratefully thank Loek Wouters and Wendy Sluijsmans for their assistance. FR and SV carried out the study, collected and analyzed the data and wrote the largest part of the paper. WJG wrote the part on pediatric endocrinology. MW and AN supervised FR and SV. Planning, processing the results and writing the paper were done under general supervision by AN and MW. This work was supported by NUTRIM, Maastricht University, Maastricht, The Netherlands.
The authors declare no conflict of interest.
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Rutters, F., Gerver, W., Nieuwenhuizen, A. et al. Sleep duration and body-weight development during puberty in a Dutch children cohort. Int J Obes 34, 1508–1514 (2010). https://doi.org/10.1038/ijo.2010.161
- sleep duration
- Tanner stage
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