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Letter to the Editor |
Department of Health Sciences, University of Jyväskylä, Jyväskylä 40014 JKL, Finland
Address correspondence to: Qingju Wang, MD, Department of Health Sciences, University of Jyvaskyla, 40014 JKL, Finland. E-mail: Qingju{at}sport.jyu.fi.
To the editor:
We agree with Dr. Moras concern regarding the common mistakes made in clinical studies in interpreting correlation results. It is true that the association between 17ß-estradiol (E2) and bone mineral density (BMD) and other bone geometric properties were relatively weak (r = 0.20.3). However, this is reasonable because, as we have mentioned in the Discussion (1), E2 is not the only factor determining the growth of bone in terms of BMD and size. It is not even the most important factor.
Dr. Mora (2) suspects that the significant relationship was due to the large number of observations. From a statistical point of view, the number of observations indeed affects significance, but does not affect the association level, which is still noteworthy.
It is true that proof of cause and effect cannot be based on an observational study alone. We are simply using the pattern of associations to infer a plausible physical mechanism. We are not claiming that the associations prove that estradiol is suppressing endosteal resportion, although there is a growing body of evidence to support such an assertion.
Hormonal influences during bone growth remain poorly understood. We hope that in the near future we can shed further light on the physiological effect of E2 and other hormones on bone mineral density and size during puberty.
Received August 19, 2004.
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