Endogenous sex steroids, weight change and rates of hip bone loss in older men: the MrOS study
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Lower levels of endogenous sex steroids or declines in these hormones may contribute to the increased rates of bone loss observed in older adults experiencing weight loss. We hypothesized that among older men with weight loss, higher rates of bone loss at the hip would be observed in men with lower baseline bioavailable sex steroids or those with greater declines in these hormones.
To test this hypothesis, body weight, hip bone mineral density (BMD) using dual energy x-ray absorptiometry and endogenous sex steroids in paired serum samples by sensitive immunoassays were measured at a baseline and at a second examination that was held an average of 1.8 years later in 1267 older men enrolled in the Osteoporotic Fractures in Men (MrOS) study.
Men experiencing weight loss had higher rates of hip bone loss than those with stable weight or weight gain within each quartile of baseline sex steroid level [p values for test of trend across weight change categories <0.010 within each quartile of bioavailable estradiol and testosterone and <0.060 within each quartile of sex hormone-binding globulin (SHBG)]. Results were similar when a change in sex steroids was substituted for baseline sex steroids in the analyses. Among men with weight loss, the rate of decline in total hip BMD showed a stepwise increase in magnitude with decreasing baseline bioavailable estradiol (p value for trend <0.040), with increasing baseline SHBG (p value for trend<0.030) and with greater decreases in bioavailable testosterone from baseline (p value for trend <0.001).
These findings support the hypothesis that the impact of weight loss in older men on rates of hip bone loss may be increased by the presence of a sex steroid insufficiency.
KeywordsBone density Estrogen Men Osteoporosis Testosterone Weight loss
Investigators in the Osteoporotic Fractures in Men (MrOS) Research Group: Coordinating Center (University of California, San Francisco and California Pacific Medical Center Research Institute): S.R. Cummings (principal investigator), M.C. Nevitt (co-investigator), D.C. Bauer (co-investigator), K.L. Stone (co-investigator), D.M. Black (co-investigator), P.M. Cawthon (project director), R. Fullman (research associate), R. Benard, T. Blackwell, J. Diehl, S. Ewing, C. Fox, M. Jaime-Chavez, E. Kwan, S. Litwack, L.Y. Lui, A. Mills, L. Palermo, J. Schneider, R. Scott, D. Tanaka, C. Yeung; Administrative Center) (Oregon Health and Sciences University: E. Orwoll (principal investigator), L. Marshall (co-investigator), J. Babich Blank (project director), L. Lambert, B. Chan, D. Neevel, J. Mougey, L. Press; University of Alabama, Birmingham: C.E. Lewis (principal investigator), J. Shikany (co-investigator), P. Johnson (project director), E. Clavino, C. Oden, N. Webb, K. Hardy, S. Felder, P. Grayson, J. Wilkoff, J. King, T. Johnsey, J. Thompson; University of Minnesota: K. Ensrud (principal investigator), H. Fink (co-investigator), D. King (program manager), N. Michaels (asst. program manager), N. Nelson (clinic coordinator), C. Bird, D. Blanks, F. Imker-Witte, K. Moen, M. Paudel, M. Slindee; Stanford University: M. Stefanick (principal investigator), A. Hoffman (co-investigator), E. Moore (project director), K. Kent, B. Malig, S. Wong; University of Pittsburgh: J. Cauley (principal investigator), J. Zmuda (co-investigator), M. Danielson, L. Harper (project director), L. Buck (clinic coordinator), M. Nasim, D. Cusick, D. Moore, M. Gorecki, D. Lee, N. Watson, C. Bashada, C. Newman, G. Engleka; University of California, San Diego: E. Barrett-Connor (principal investigator), T. Dam (co-investigator), ML Carrion-Petersen (project director), P. Miller, N. Kamantigue, S. Szerdi, G. Reno.
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