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Department of Medicine (I.R.R., J.L., D.W., A.H., M.B., G.D.G., A.B.G.), University of Auckland, New Zealand; and LabPlus (J.S.D.), Auckland Hospital, New Zealand
Address all correspondence and requests for reprints to: Dr. I. R. Reid, Department of Medicine, University of Auckland, Private Bag 92019, Auckland, New Zealand. E-mail: i.reid{at}auckland.ac.nz.
Introduction: The central nervous system has been demonstrated to regulate bone mass in mice, possibly via the ß2-adrenoreceptors on osteoblasts. ß-blockers increase bone mass in mice, and some observational studies have suggested a beneficial effect of these drugs on bone in humans
Experimental Subjects: We studied 41 normal postmenopausal women.
Materials and Methods: We conducted a randomized, placebo- controlled trial, comparing the effects on bone markers of propranolol 160 mg/d and placebo over 3 months.
Results: Serum osteocalcin declined by almost 20% in the first 2 wk of propranolol treatment, and this effect increased over time (P < 0.0001). Other osteoblast markers, procollagen type-I N-terminal propeptide and total alkaline phosphatase activity, were not significantly changed by propranolol. Urine free deoxypyridinoline declined by approximately 10% between 0 and 6 wk (P = 0.019) in the ß-blocker group and was stable thereafter. Serum C-terminal telopeptide of type I collagen also showed a small decrease, but this was not significantly different between groups. Serum albumin concentrations decreased by more than 2 g/liter in the first 2 wk of propranolol treatment, remaining stable subsequently (P = 0.007). Serum creatinine tended to increase in the propranolol group (P = 0.06), as did weight. Bone densities in the lumbar spine and total proximal femur did not change significantly in either group.
Conclusions: The present study provides no evidence that ß-blocker drugs stimulate bone formation; if anything, propranolol reduces osteoblast activity. It also influences renal function and fluid balance, effects that might indirectly affect bone metabolism. Current evidence does not justify the use of ß-blockers for treatment of osteoporosis.
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A. Grey, M. Bolland, G. Gamble, D. Wattie, A. Horne, J. Davidson, and I. R. Reid The Peroxisome Proliferator-Activated Receptor-{gamma} Agonist Rosiglitazone Decreases Bone Formation and Bone Mineral Density in Healthy Postmenopausal Women: A Randomized, Controlled Trial J. Clin. Endocrinol. Metab., April 1, 2007; 92(4): 1305 - 1310. [Abstract] [Full Text] [PDF] |
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