Cited by 156Bone health and osteoporosis researchBone Metabolism and DiseasesMenopause: Health Impacts and Treatments

β-Blocker Use, BMD, and Fractures in the Study of Osteoporotic Fractures

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Reid, Ian R, Gamble, Gregory D, Grey, Andrew B, Black, Dennis M, Ensrud, Kristine E, Browner, Warren S, Bauer, Douglas C·2005·Journal of Bone and Mineral Research

Abstract

A role for osteoblastic β-adrenoreceptors in bone regulation is suggested by the finding that β-blockers increase bone mass in mice. We studied the association of β-blocker use with BMD and fractures in the Study of Osteoporotic Fractures. β-blocker use and BMD are unrelated in this cohort, and associations with fracture risk are inconsistent. Introduction: The central nervous system has been shown to regulate bone mass in mice, possibly by way of the β2-adrenoreceptors on osteoblasts. β-blockers have been shown to increase bone mass in mice. Because these agents are widely used therapeutically, it is possible that they may influence fracture epidemiology in humans, and they are a potential therapy for osteoporosis. Materials and Methods: We have studied the association of β-blocker use with BMD and fracture rates in the Study of Osteoporotic Fractures. β-blocker use was recorded at the fourth visit, in 8412 women, of whom 1099 were users, and these women were followed for 7 years. Results: Users had significantly higher weight, more thiazide use, more estrogen use, less glucocorticoid use, more statin use, and more hypertension than nonusers, and they smoked less. Total hip BMD at the fourth visit was higher in the β-blocker users (0.746 versus 0.735 g/cm2, p = 0.02), but adjustment for weight alone, or together with these other variables, eliminated this difference (p = 0.62). There was no effect of β-blocker use on loss of hip BMD over a mean follow-up of 4 years (p = 0.48). Os calcis BMD at visit 4 was also higher in those taking β-blockers (0.385 versus 0.375 g/cm2, p = 0.005), but weight adjustment eliminated this difference (p = 0.14). The frequencies of hip or any fracture (since age 50) were similar in users and nonusers (p = 0.80 and p = 0.51, respectively). Over a mean follow-up of 7 years, there were 2167 total fractures, including 431 at the wrist and 585 at the hip. Among β-blocker users, hazards ratios were 0.92 (0.81, 1.05) for any fracture, 0.74 (0.54, 1.01) for wrist fracture, and 0.76 (0.58, 0.99) for hip fracture. Adjustment for weight and other factors previously shown to influence hip fracture incidence in this cohort made little difference to the outcome. When fracture data were analyzed for nonselective and β1-selective agents separately, trends toward fewer fractures were confined to the users of selective β1-blockers. Conclusions: β-blocker use and BMD are unrelated in this cohort, and associations with fracture risk are inconsistent. Therefore, a history of use of these drugs is not useful in assessing fracture risk, nor do they have a role in osteoporosis management at this time. The relationship between β-blocker use and hip fracture deserves further study.

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  • In mice, leptin deficiency or resistance is linked to high bone mineral density even though gonadal function is reduced.

    “Leptin deficiency or resistance is associated with high BMD in mice despite the fact that gonadal function is diminished (103).”

    From Pathogenesis of osteoporosis: concepts, conflicts, and prospects (2005) · cites this paper as [103]

    The Introduction (page unavailable) says leptin affects bone formation and bone mass in mice, but does not discuss leptin deficiency or resistance, high BMD in those mice, or diminished gonadal function. Searches for the claimed combination and for gonadal function found no passage addressing it. (LLM, conf=0.72)

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Authors
Reid, I. R., Gamble, G. D., Grey, A. B., Black, D. M., Ensrud, K. E., Browner, W. S., & Bauer, D. C.
Affiliations
  • University of Auckland (NZ)
  • Department of Medicine, University of Auckland, Auckland, New Zealand
  • University of California, San Francisco (US)
  • University of Minnesota (US)
Corresponding author
Reid, Ian R
Venue
Journal of Bone and Mineral Research
Published
2005-04-01
Volume
20
Issue
4
Pages
613-618
ISSN
  • 0884-0431 (ISSN-L)
  • 1523-4681
OpenAlex
W2046327104
Cited by
156
References
19
Citations by year
2026: 5 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 2 · 2016: 5 · 2015: 9 · 2014: 3 · 2013: 13 · 2012: 14
FWCI
17.46
Type
journal article
Language
en
Open access
Locations
  • Journal of Bone and Mineral Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Public Health Service
  • Health Research Council of New Zealand
  • National Institute on Aging (AG05394, AG-05407)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR035584, AR35583, AR-35584, AR 35582, R01AR035582, R01AR035583)
Topics
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Menopause: Health Impacts and Treatments
Keywords
beta-blockers, bone mineral density, osteoporotic fractures, hip fracture, wrist fractures, bone mass regulation, Study of Osteoporotic Fractures, women, thiazide diuretics, glucocorticoids, estrogen use, statins, hypertension, osteoporosis treatment, fracture risk factors
MeSH terms
Adrenergic beta-Antagonists, Aged, Bone and Bones, Female, Fractures, Spontaneous, Humans, Osteoporosis, Bone Density, Risk Assessment

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