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|Title:||Loading and bone fragility.||Austin Authors:||Seeman, Ego||Affiliation:||Endocrine Unit, Department of Medicine, Austin Hospital, University of Melbourne, Melbourne, Australia||Issue Date:||2005||Publication information:||Journal of Bone and Mineral Metabolism; 23 Suppl(): 23-9||Abstract:||Data from retrospective and prospective observational and case-control studies suggest that activity is associated with reduced fracture risk, but consistently replicated bias may be responsible for this desired endpoint. Exercise during growth is likely to build a larger and stronger skeleton. However, cessation of exercise may erode the benefits. Modeling changes produced by exercise during growth may be permanent; remodeling changes may not be. Exercise during adulthood produces small increments in BMD or may prevent bone loss. Absence of evidence is not evidence of absence of effect, but the null hypothesis that exercise has no effect on fracture rates in old age cannot be rejected by any published data. Proof requires demonstration of a reduction in spine and hip fractures in well-designed and well-executed prospective randomized studies; none exists. Blinded studies cannot be done, but open trials can and should be done.||Gov't Doc #:||15984410||URI:||http://ahro.austin.org.au/austinjspui/handle/1/9950||URL:||https://pubmed.ncbi.nlm.nih.gov/15984410||Type:||Journal Article||Subjects:||Age Factors
Fractures, Bone.drug therapy.prevention & control
Osteoporosis.drug therapy.prevention & control
|Appears in Collections:||Journal articles|
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