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Volume 118, Issue 12, Pages 1414.e1-1414.e5 (December 2005)


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Lipid levels and bone mineral density

Daniel H. Solomon, MD, MPHabaCorresponding Author Informationemail address, Jerry Avorn, MDa, Claire F. Canning, MAa, Philip S. Wang, MD, DrPHac

Abstract 

Purpose

There has been considerable debate about the potential relationship between the use of statin lipid-lowering drugs and fracture risk; several observational studies suggest a protective effect but no randomized controlled trials have confirmed such a benefit. Because statins are given preferentially to persons with hyperlipidemia, if lipid levels were associated with bone mineral density, this could explain the discrepancy between epidemiological observations and randomized controlled trials. The aim of this study was to examine the relationship between lipid levels and bone mineral density.

Subjects and methods

We included the 13592 participants in the National Health and Nutritional Examination Survey (NHANES) III who had bone mineral density and lipid levels measured; participants who reported the use of a lipid-lowering therapy were excluded. We examined the unadjusted bone mineral density across quintiles of total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL). We then constructed multivariable models, including age, sex, body mass index, and other potential confounders.

Results

In crude analyses, higher total cholesterol and LDL levels were associated with lower bone mineral densities (both P values for trend <.001), whereas higher HDL levels were associated with higher bone mineral densities (P value for trend <.001). However, in fully adjusted models, there was no significant relationship between total cholesterol, LDL, or HDL levels and bone mineral density (all P values for trend >.1).

Conclusions

These results do not support a relationship between lipid levels and bone mineral density.

a Division of Pharmacoepidemiology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass

b Division of Rheumatology, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass

c Department of Psychiatry, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass

Corresponding Author InformationRequests for reprints should be addressed to Daniel H. Solomon, MD, MPH, Division of Pharmacoepidemiology, Brigham and Women’s Hospital, 1620 Tremont Street, Suite 3030, Boston, MA 02120

a Dr. Solomon receives salary support from NIH AR-48616, the Arthritis Foundation, and the Engalitcheff Arthritis Outcomes Initiative.

PII: S0002-9343(05)00625-X

doi:10.1016/j.amjmed.2005.07.031


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