Assessing causality between obstructive sleep apnea with the dyslipidemia and osteoporosis: a Mendelian randomization study.

Front Genet

Department of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Fujian Medical University, Center of Respiratory Medicine of Fujian, Quanzhou, China.

Published: June 2024

AI Article Synopsis

  • The study investigates the causal links between Obstructive Sleep Apnea (OSA), dyslipidemia (abnormal lipid levels), and osteoporosis using Mendelian Randomization techniques.
  • Researchers applied a two-sample MR approach, analyzing genetic data from large cohorts, and found that OSA significantly impacts triglyceride levels and reduces high-density lipoprotein cholesterol (HDL-C), while no causal relationship was found between dyslipidemia and OSA or between OSA and osteoporosis.
  • The findings suggest that there is a causal relationship between OSA and dyslipidemia, indicating a need for targeted management of OSA to help treat lipid-related issues, while further investigation is needed for the relationship with osteoporosis.

Article Abstract

Purpose: This study aims to assess the causal relationship between Obstructive Sleep Apnea (OSA), dyslipidemia, and osteoporosis using Mendelian Randomization (MR) techniques.

Methods: Utilizing a two-sample MR approach, the study examines the causal relationship between dyslipidemia and osteoporosis. Multivariable MR analyses were used to test the independence of the causal association of dyslipidemia with OSA. Single nucleotide polymorphisms (SNPs) were selected as instrumental variables based on genome-wide significance, independence, and linkage disequilibrium criteria. The data were sourced from publicly available Genome-Wide Association Studies (GWAS) of OSA ( = 375,657) from the FinnGen Consortium, the Global Lipids Genetics Consortium of dyslipidemia ( = 188,577) and the UK Biobank for osteoporosis ( = 456,348).

Results: The MR analysis identified a significant positive association between genetically predicted OSA and triglyceride levels (OR: 1.15, 95% CI: 1.04-1.26, = 0.006) and a negative correlation with high-density lipoprotein cholesterol (HDL-C) (OR: 0.84, 95% CI: 0.77-0.93, = 0.0003). Conversely, no causal relationship was found between dyslipidemia (total cholesterol, triglycerides, HDL-C, and low-density lipoprotein cholesterol) and OSA or the relationship between OSA and osteoporosis.

Conclusion: The study provides evidence of a causal relationship between OSA and dyslipidemia, highlighting the need for targeted prevention and management strategies for OSA to address lipid abnormalities. The absence of a causal link with osteoporosis and in the reverse direction emphasizes the need for further research in this area.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11222592PMC
http://dx.doi.org/10.3389/fgene.2024.1359108DOI Listing

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