The American Journal of Medicine
Volume 119, Issue 5 , Pages 426-433, May 2006

Estradiol, Testosterone, and the Risk for Hip Fractures in Elderly Men from the Framingham Study

  • Shreyasee Amin, MDCM, MPH

      Affiliations

    • Boston University Clinical Epidemiology Research and Training Unit, Department of Medicine, Boston University School of Medicine, Boston, Mass
    • Corresponding Author InformationRequests for reprints should be addressed to Shreyasee Amin, MDCM, FRCP(C), MPH, Division of Rheumatology, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905
  • ,
  • Yuqinq Zhang, DSc

      Affiliations

    • Boston University Clinical Epidemiology Research and Training Unit, Department of Medicine, Boston University School of Medicine, Boston, Mass
  • ,
  • David T. Felson, MD, MPH

      Affiliations

    • Boston University Clinical Epidemiology Research and Training Unit, Department of Medicine, Boston University School of Medicine, Boston, Mass
  • ,
  • Clark T. Sawin, MD

      Affiliations

    • Office of History and Archives, Veterans Administration Headquarters, Washington, DC (posthumous)
  • ,
  • Marian T. Hannan, DSc, MPH

      Affiliations

    • Institute for Aging Research, Hebrew Senior Life, Harvard Medical School, Boston, Mass
  • ,
  • Peter W.F. Wilson, MD

      Affiliations

    • National Heart Lung and Blood Institute’s Framingham Heart Study, Framingham, Mass
  • ,
  • Douglas P. Kiel, MD, MPH

      Affiliations

    • Institute for Aging Research, Hebrew Senior Life, Harvard Medical School, Boston, Mass

Received 8 July 2005; accepted 25 October 2005.

Abstract 

Background

Low serum estradiol has been more strongly associated with low bone mineral density in elderly men than has testosterone, but its association with incident hip fracture is unknown. We examined whether low estradiol increases the risk for future hip fracture among men and explored whether testosterone levels influence this risk.

Methods

We examined 793 men (mean age = 71 years) evaluated between 1981 and 1983, who had estradiol measures and no history of hip fracture, and followed until the end of 1999. Total estradiol and testosterone were measured between 1981 and 1983. Hip fractures were identified and confirmed through medical records review through the end of 1999. We created 3 groups of men based on estradiol levels and performed a Cox-proportional hazards model to examine the risk for incident hip fracture, adjusted for age, body mass index, height, and smoking status. We performed similar analyses based on testosterone levels, and then based on both estradiol and testosterone levels together.

Results

There were 39 men who sustained an atraumatic hip fracture over follow-up. Incidence rates for hip fracture (per 1000 person-years) were 11.0, 3.4, and 3.9 for the low (2.0-18.1 pg/mL [7-67 pmol/L]), middle (18.2-34.2 pg/mL [67-125 pmol/L]), and high (≥34.3 pg/mL [≥126 pmol/L]) estradiol groups, respectively. With adjustment for age, body mass index, height, and smoking status, the adjusted hazard ratios for men in the low and middle estradiol groups, relative to the high group, were 3.1 (95% confidence interval [CI], 1.4-6.9) and 0.9 (95% CI, 0.4-2.0), respectively. In similar adjusted analyses evaluating men by their testosterone levels, we found no significant increased risk for hip fracture. However, in analyses in which we grouped men by both estradiol and testosterone levels, we found that men with both low estradiol and low testosterone levels had the greatest risk for hip fracture (adjusted hazard ratio: 6.5, 95% CI, 2.9-14.3).

Conclusion

Men with low estradiol levels are at an increased risk for future hip fracture. Men with both low estradiol and low testosterone levels seem to be at greatest risk for hip fracture.

Keywords:  Estradiol , Testosterone , Male , Hip fracture , Cohort study

 

 This work is from the National Heart, Lung, and Blood Institute’s Framingham Heart Study, supported by National Institutes of Health/National Heart, Lung, and Blood Institute contract N01-HC-25195. This work was also supported in part by grant AR47785 and AR/AG41398 from the National Institutes of Health, and by the Veterans Administration Research Institute, Boston VAMC. Dr Amin’s work was supported by a Physician Scientist Development Award from the Arthritis Foundation and, in part, by Merck Frosst Canada Inc.

PII: S0002-9343(05)01053-3

doi:10.1016/j.amjmed.2005.10.048

The American Journal of Medicine
Volume 119, Issue 5 , Pages 426-433, May 2006