Swaroop D Mistry1, Gina N Woods2, Sigurdur Sigurdsson3, Susan K Ewing4, Trisha F Hue5, Gudny Eiriksdottir6, Kaipin Xu7, Joan F Hilton8, Deborah M Kado9, Vilmundur Gudnason10, Tamara B Harris11, Clifford J Rosen12, Thomas F Lang13, Xiaojuan Li14, Ann V Schwartz15. 1. Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94158, USA. Electronic address: Swaroop.Mistry@ucsf.edu. 2. Department of Medicine, University of California San Diego, CA 92093, USA. Electronic address: gwoods@ucsd.edu. 3. Icelandic Heart Association Research Institute, Iceland. Electronic address: sigurdur@hjarta.is. 4. Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94158, USA. Electronic address: sewing@psg.ucsf.edu. 5. Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94158, USA. Electronic address: thue@psg.ucsf.edu. 6. Icelandic Heart Association Research Institute, Iceland. Electronic address: gudny@hjarta.is. 7. Department of Radiology and Biomedical Imaging, University of California San Francisco, CA 94107, USA. Electronic address: Kaipin.Xu@ucsf.edu. 8. Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94158, USA. Electronic address: Joan.Hilton@ucsf.edu. 9. Department of Family Medicine and Family Health, University of California San Diego, CA 92093, USA. Electronic address: dkado@ucsd.edu. 10. Icelandic Heart Association Research Institute, Iceland. Electronic address: villi@hjarta.is. 11. Intramural Research Program, National Institute of Aging, 20892, USA. Electronic address: Harris99@nia.nih.gov. 12. Maine Medical Center Research Institute, Portland, ME 04102, USA. Electronic address: cjrofen@gmail.com. 13. Department of Radiology and Biomedical Imaging, University of California San Francisco, CA 94107, USA. Electronic address: Thomas.Lang@ucsf.edu. 14. Department of Radiology and Biomedical Imaging, University of California San Francisco, CA 94107, USA. Electronic address: Xiaojuan.Li@ucsf.edu. 15. Department of Epidemiology and Biostatistics, University of California San Francisco, CA 94158, USA. Electronic address: aschwartz@psg.ucsf.edu.
Abstract
CONTEXT: Higher bone marrow fat (BMF)1 is associated with osteoporosis and reduced hematopoiesis. Exogenous estradiol reduces BMF in older women, but effects of endogenous sex hormones are unknown. OBJECTIVE: To determine if endogenous sex hormones are associated with BMF in older men and women. DESIGN, SETTING AND PARTICIPANTS: Cross-sectional study in the Age Gene/Environment Susceptibility (AGES) Reykjavik cohort. Participants using medications that may affect BMF were excluded. MAIN OUTCOME MEASURES: Vertebral BMF was measured with magnetic resonance spectroscopy. Estradiol, testosterone and sex hormone binding globulin were measured on archived serum. Linear regression models were adjusted for age, total percent body fat and visit window. RESULTS: Analyses included 244 men and 226 women, mean age 81.5 (SD 4.1) years. Mean BMF was 54.1% (SD 8.6) (men) and 54.7% (SD 8.1) (women). In adjusted models, per 1pg/ml increase in total estradiol, there was a statistically significant 0.26% decrease in BMF in men (95% CI: -0.41, -0.11) and a non-significant 0.20% decrease in women (95% CI: -0.55, 0.15), with no evidence of interaction by gender (p=0.88). Per 10ng/dl increase in total testosterone, there was a significant 0.10% decrease in BMF in men (95% CI: -0.17, -0.03) and a non-significant 0.13% (95% CI: -0.79, 0.53) decrease in women, with no evidence of interaction by gender (p=0.97). CONCLUSION: Higher bone marrow fat is associated with lower total estradiol and testosterone levels in older men, with a similar but statistically non-significant association in older women. Sex hormone levels appear to play a role in the regulation of bone marrow fat in older adults.
CONTEXT: Higher bone marrow fat (BMF)1 is associated with osteoporosis and reduced hematopoiesis. Exogenous estradiol reduces BMF in older women, but effects of endogenous sex hormones are unknown. OBJECTIVE: To determine if endogenous sex hormones are associated with BMF in older men and women. DESIGN, SETTING AND PARTICIPANTS: Cross-sectional study in the Age Gene/Environment Susceptibility (AGES) Reykjavik cohort. Participants using medications that may affect BMF were excluded. MAIN OUTCOME MEASURES: Vertebral BMF was measured with magnetic resonance spectroscopy. Estradiol, testosterone and sex hormone binding globulin were measured on archived serum. Linear regression models were adjusted for age, total percent body fat and visit window. RESULTS: Analyses included 244 men and 226 women, mean age 81.5 (SD 4.1) years. Mean BMF was 54.1% (SD 8.6) (men) and 54.7% (SD 8.1) (women). In adjusted models, per 1pg/ml increase in total estradiol, there was a statistically significant 0.26% decrease in BMF in men (95% CI: -0.41, -0.11) and a non-significant 0.20% decrease in women (95% CI: -0.55, 0.15), with no evidence of interaction by gender (p=0.88). Per 10ng/dl increase in total testosterone, there was a significant 0.10% decrease in BMF in men (95% CI: -0.17, -0.03) and a non-significant 0.13% (95% CI: -0.79, 0.53) decrease in women, with no evidence of interaction by gender (p=0.97). CONCLUSION: Higher bone marrow fat is associated with lower total estradiol and testosterone levels in older men, with a similar but statistically non-significant association in older women. Sex hormone levels appear to play a role in the regulation of bone marrow fat in older adults.
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