Objective: To test the hypothesis that the decline in femoral bone mass associated with healthy aging is partially accounted for by deficiency of the growth hormone-insulin-like growth factor-I (IGF-I) axis.
Design: Cross-sectional study.
Study participants: A sample of 245 community-dwelling healthy women aged 70 and older. Exclusion criteria were diseases or medications known to affect the musculoskeletal system or the somatotrophic axis.
Measurements: Serum levels of IGF-I, calcitriol, and osteocalcin were determined by radioimmunoassay; serum calcidiol was measured by competitive binding assay, and serum parathyroid hormone (PTH) was assessed immunochemically. Urinary pyridinium crosslinks were measured by fluorescent detection after high-pressure liquid chromatography. Isometric and isokinetic quadriceps strength was evaluated using an isokinetic dynamometer. Bone density (BMD) was assessed by dual-energy X-ray absorptiometry at the proximal femur. Multiple regression was used to adjust for potential confounders.
Results: At the proximal femur, BMD declined by 0.59-0.84% per year. In addition to body mass index and muscle strength, serum IGF-I was found to be an independent predictor of BMD at all femoral sites.
Conclusion: The data support the hypothesis that circulating IGF-I not only reflects the integrated growth hormone secretion but also has a direct role in the endocrine regulation of bone remodeling. The present findings support the need for further studies to assess the potential of IGF-I in attenuating age-related femoral bone loss.