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Published on: January 29, 2018
Positive effects of low LDL-C and statins on bone mineral density: an integrated epidemiological observation analysis
Gloria Hoi-Yee Li1, Ching-Lung Cheung1,2,3, Philip Chun-Ming Au1
1Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong.
Insights
Low-density lipoprotein cholesterol (LDL-C) is causally linked to lower bone mineral density (BMD). LDL-C-lowering drugs, like statins, appear to increase BMD, suggesting a protective effect on bone health.
Area of Science:
- Bone Metabolism and Endocrinology
- Cardiovascular Health and Osteoporosis Link
- Genetic Epidemiology of Metabolic Diseases
Background:
- The relationship between low-density lipoprotein cholesterol (LDL-C) and osteoporosis is debated, with unclear effects of LDL-C-lowering medications on bone.
- Investigating the causal link between LDL-C and bone metabolism is crucial for understanding osteoporosis pathogenesis and treatment.
Purpose of the Study:
- To determine if LDL-C is causally associated with bone mineral density (BMD).
- To assess the impact of LDL-C-lowering drugs on BMD using genetic proxies.
Main Methods:
- Epidemiological analyses were conducted on the US NHANES III and Hong Kong Osteoporosis Study (HKOS) cohorts.
- Two-sample Mendelian randomization (MR) was employed using large-scale genome-wide association study (GWAS) data for lipids and BMD.
- Genetic proxies for statins were used to evaluate their effect on BMD.
Main Results:
- Observational studies showed decreased LDL-C associated with increased femoral neck and lumbar spine BMD.
- MR analysis revealed a causal inverse relationship between genetically predicted LDL-C and total body BMD (TB-BMD) and estimated BMD (eBMD).
- Genetic proxies for statins were associated with increased TB-BMD and eBMD.
Conclusions:
- A negative causal association exists between LDL-C levels and BMD.
- The LDL-C-lowering effect of statins is linked to increased BMD, indicating a potential bone-protective role.
Background:
Low-density lipoprotein cholesterol (LDL-C) is suggested to play a role in osteoporosis but its association with bone metabolism remains unclear. Effects of LDL-C-lowering drugs on bone are also controversial. We aim to determine whether LDL-C is linked causally to bone mineral density (BMD) and assess the effects of LDL-C-lowering drugs on BMD.
Methods:
Association between blood lipid levels and BMD was examined by epidemiological observation analyses in a US representative cohort NHANES III (n = 3638) and the Hong Kong Osteoporosis Study (HKOS; n = 1128). Two-sample Mendelian randomization (MR), employing genetic data from a large-scale genome-wide association study (GWAS) of blood lipids (n = 188 577), total body BMD (TB-BMD) (n = 66 628) and estimated BMD (eBMD) (n= 142 487), was performed to infer causality between LDL-C and BMD. Genetic proxies for LDL-C-lowering drugs were used to examine the drugs' effects on BMD.
Results:
In the NHANES III cohort, each standard deviation (SD) decrease in LDL-C was associated with a 0.045 SD increase in femoral neck BMD (95% CI: 0.009 - 0.081; P = 0.015). A similar increase in BMD was observed in the HKOS at femoral neck and lumbar spine. In MR analysis, a decrease in genetically predicted LDL-C was associated with an increase in TB-BMD {estimate per SD decrease, 0.038 [95% confidence interval (CI): 0.002 - 0.074]; P = 0.038} and eBMD [0.076 (0.042 - 0.111); P = 1.20x10-5]. Reduction in TB-BMD was causally associated with increased LDL-C [0.035 (0.033 - 0.066); P = 0.034]. Statins' LDL-C-lowering proxies were associated with increased TB-BMD [0.18 (0.044 - 0.316); P = 9.600x10-3] and eBMD [0.143 (0.062 - 0.223); P = 5.165x10-4].
Conclusions:
Negative causal association exists between LDL-C level and BMD. Statins' LDL-C-lowering effect increases BMD, suggesting their protective effect on bone.
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