Skeletal Status and Bone Turnover in Overweight Young Men with and without Sleep Apnea Syndrome
Obesity is a worldwide epidemic increasing at an alarming rate among youth who are facing similar health problems as adults. Sleep Apnea Syndrome (SAS) is an underdiagnosed comorbidity of obesity, characterized by repetitive nocturnal interruptions in breathing. Obesity is associated with delayed skeletal maturation in overweight youth, but mechanisms contributing to this problem are unclear. Obesity and SAS both have been shown to disrupt regulatory hormones and cytokines that influence bone accretion during adolescence. PURPOSE: The purpose of this study was to assess the combined effects of excess body weight and SAS on bone mineral density (BMD) and content (BMC), bone turnover, and on the regulatory hormones leptin and IGF-1 known to potentially influence bone accretion during adolescence. METHODS: Men aged 18-28 years were assigned to groups as follows: normal weight controls (CON: AHI <3, n=8); overweight without SAS (OWT: BMI < 26 kg/m2 and AHI <3, n=9); and overweight with SAS (SAS: BMI >26 kg/m2 and AHI >5, n=8). The apnea/hypopnea index (AHI) expresses the score for disrupted nighttime breathing events/hr and was obtained in this study with results from a home sleep screening test. Health history and Epworth Sleepiness Scale (ESS) questionnaires also were administered. Bone mineral parameters and body composition variables were measured with dual-energy X-ray absorptiometry. Serum osteocalcin, leptin, IGF-1, and NTx-1 were measured, respectively, by radioimmunoassay and enzyme-linked immunoabsorbent assay. RESULTS: Fat-free mass, intra-abdominal fat, and fat mass were higher in the SAS and OWT groups (p<0.03). ESS scores revealed that SAS individuals were sleepier than CON and OWT groups (p<0.009). Total body and site-specific BMD and BMC values (lumbar spine, hip, and forearm) were similar between groups and did not relate to the estimated AHI score. Serum OC and NTx-1 did not differ between groups. Leptin levels were 30% higher in OWT and SAS than in the CON group (p<0.02), but did not correlate with the AHI score. Across all subjects (n=25), only lumbar spine BMC (p<0.005) was correlated to AHI (r=-.52; p<0.01). The preponderance of this relationship between AHI and lumbar spine BMC was attributable to the close inverse association of these two variables within the SAS group (r = -.81; p<0.001). CONCLUSION: The effects of SAS were not influenced by the amount of whole-body, intra-abdominal adiposity or lean body mass. Neither leptin nor IGF-1 predicted bone status across all groups. Daytime fatigue and sleepiness, a cardinal symptom of SAS, combined with overweight may contribute to lower lumbar BMC by chronically reducing weight-bearing physical activity and thereby reduce exposure time for mechanical loading of the spine in affected individuals. Further research is needed to explore the biochemical, physiological, and apparently the physical activity implications of SAS on skeletal status and turnover.