Article

The association between obstructive sleep apnea and dietary choices among obese individuals during middle to late childhood.

Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Sleep Medicine (Impact Factor: 3.1). 08/2011; 12(8):797-9. DOI: 10.1016/j.sleep.2010.12.020
Source: PubMed

ABSTRACT Determine whether obstructive sleep apnea (OSA) is associated with the dietary choices of obese individuals during middle- to late-childhood. It was hypothesized that OSA would be associated with increased caloric content of a dinner order, particularly with high carbohydrate food choices. Secondarily, we examined the relationships between sleep duration and dietary choices.
42 obese subjects aged 10-16.9 years participated in a cross-sectional study that involved systematic collection of sleep duration (based on actigraphy), presence and severity of obstructive sleep apnea (obstructive apnea+hypopnea index [AHI] from inpatient polysomnography) and the macronutrient content of dinners ordered from a standardized hospital menu the evening before the polysomnogram.
Primary analyses using Spearman rank-order correlations found that AHI was significantly associated with total calories, as well as grams of fat and carbohydrate, but not protein. These macronutrient variables did not correlate with sleep duration across a week, nor the night before the meal. Findings were unchanged after correcting for age- and sex-adjusted BMI.
More severe OSA appears to be associated with an increased preference for calorie-dense foods that are high in fat and carbohydrates in a manner that is independent of degree of obesity. Although this novel finding awaits replication, it has potential implications for the clinical care of obese youth and individuals with OSA, adds to the limited data that relate sleep to dietary choices and may have implications for OSA-related morbidity.

0 Followers
 · 
66 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Data from cross-sectional and longitudinal studies have illustrated a relationship between short sleep duration (SSD) and weight gain. Individuals with SSD are heavier and gain more weight over time than normal-duration sleepers. This sleep-obesity relationship may have consequences for obesity treatments, as it appears that short sleepers have reduced ability to lose weight. Laboratory-based clinical studies found that experimental sleep restriction affects energy expenditure and intake, possibly providing a mechanistic explanation for the weight gain observed in chronic short sleepers. Specifically, compared to normal sleep duration, sleep restriction increases food intake beyond the energetic costs of increased time spent awake. Reasons for this increased energy intake after sleep restriction are unclear but may include disrupted appetite-regulating hormones, altered brain mechanisms involved in the hedonic aspects of appetite, and/or changes in sleep quality and architecture. Obstructive sleep apnea (OSA) is a disorder at the intersection of sleep and obesity, and the characteristics of the disorder illustrate many of the effects of sleep disturbances on body weight and vice versa. Specifically, while obesity is among the main risk factors for OSA, the disorder itself and its associated disturbances in sleep quality and architecture seem to alter energy balance parameters and may induce further weight gain. Several intervention trials have shown that weight loss is associated with reduced OSA severity. Thus, weight loss may improve sleep, and these improvements may promote further weight loss. Future studies should establish whether increasing sleep duration/improving sleep quality can induce weight loss.
    Hormone molecular biology and clinical investigation 01/2014; 17(1):29-37. DOI:10.1515/hmbci-2013-0066
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obstructive sleep apnea (OSA) is a common health problem, particularly in obese children, in whom a vicious cycle of obesity and OSA interdependencies promotes increased food intake. G protein-coupled receptor 120 (GPR 120) is a long-chain free fatty acid (FFA) receptor that plays an important role in energy homeostasis, and protects against insulin resistance and systemic inflammation. We hypothesized that GPR 120 levels would be reduced in children with OSA, particularly among obese children. Cross-sectional prospectively recruited cohort. Academic pediatric sleep program. Two hundred twenty-six children (mean age: 7.0 ± 2.1 y) underwent overnight polysomnographic evaluation and a fasting blood draw the morning after the sleep study. In addition to lipid profile, homeostasis model assessment of insulin resistance (HOMA-IR) and high-sensitivity C-reactive protein (hsCRP) assays, monocyte GPR 120 expression, and plasma GPR 120 levels were assessed using quantitative polymerase chain reaction and enzyme-linked immunosorbent assay kits. Obese children and those with OSA had significantly lower GPR 120 monocyte expression and plasma GPR 120 levels. Furthermore, when both obesity and OSA were present, GPR 120 levels were lowest. Linear associations emerged between GPR 120 plasma levels and body mass index (BMI) z score, as well as with apnea-hypopnea index (AHI), saturation of peripheral oxygen (SpO2) nadir, and respiratory arousal index (RAI), with RAI remaining statistically significant when controlling for age, ethnicity, sex, and BMI z score (P < 0.001). Similarly, HOMA-IR was significantly associated with GPR 120 levels, but neither low density lipoprotein nor high density lipoprotein cholesterol or hsCRP levels exhibited significant correlations. G protein-coupled receptor 120 (GPR 120) levels are reduced in pediatric OSA and obesity (particularly when both are present) and may play a role in modulating the degree of insulin resistance. The short- and long-term significance of reduced GPR 120 relative to food intake and glycemic deregulation remains undefined. Gozal D, Kheirandish-Gozal L, Carreras A, Khalyfa A, Peris E. Obstructive sleep apnea and obesity are associated with reduced GPR 120 plasma levels in children. SLEEP 2014;37(5):935-941.
    Sleep 05/2014; 37(5):935-941. DOI:10.5665/sleep.3664 · 5.06 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The impact of obstructive sleep apnoea (OSA) treatment with CPAP on weight is not clear. This meta-analysis was designed to assess whether OSA treatment with CPAP promotes changes in body mass index (BMI) and weight. We searched PubMed, SCOPUS and Cochrane Central Register electronic databases through 1 October 2013 (including papers in press at that time), without language restrictions. We identified randomised trials of CPAP versus controls with a minimum treatment duration of 4 weeks that objectively measured BMI. Data were independently abstracted and reviewed by two investigators using a standardised protocol. We included a total of 3181 patients from 25 randomised trials that measured BMI and weight. All studies enrolled mainly overweight and obese patients. The fixed-effects meta-analysis revealed that CPAP promoted significant increase on BMI (Hedges' g=0.14, 95% CI 0.07 to 0.21, I(2)=16.2%) and weight (Hedges' g=0.17, 95% CI 0.10 to 0.24, I(2)=0%). The funnel plot revealed low risk of publication bias. Meta-regression analyses including age, gender, baseline BMI, baseline weight, OSA severity, CPAP compliance, use of sham CPAP, study duration, study design (crossover/parallel), study origin (Western/Eastern), recommendation for dietary changes or physical activity, revealed that no single predictor influenced the main outcome for weight. Baseline weight was a predictor of increased BMI after CPAP. OSA treatment with CPAP promotes significant increase in BMI and weight. Additional therapies for body weight reduction must be recommended for overweight or obese patients with OSA initiated on CPAP. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Thorax 11/2014; 70(3). DOI:10.1136/thoraxjnl-2014-205361 · 8.56 Impact Factor

Preview

Download
0 Downloads
Available from