Investigating the impact of metabolic syndrome traits on telomere length: a Mendelian randomization study
Authors' conclusion
Overweight and obesity might promote the development of aging-related degenerative diseases by accelerating telomere shortening.
Study context
- Population
- European individuals (GWAS of anthropometric, glycemic, lipid and blood pressure traits); Leukocyte telomere length (LTL) summary data from a GWAS in the UK Biobank
- Comparison
- Genetically predicted metabolic syndrome traits and leukocyte telomere length
- Outcome
- Leukocyte telomere length (LTL)
Methodological detailsunivariable and multivariable Mendelian randomization, summary-level data
- Univariable and multivariable Mendelian randomization
- Summary-level data
Main finding
As reported in the abstract
LTL
Higher BMI associated with shorter LTL: β (95% CI −0.058 to −0.020), p = 5 × 10-5 ; equivalent to 1.70 years of age-related LTL change
−0.039
Higher LDL-C associated with longer LTL: β (95% CI 0.007 to 0.037), p = 0.003; equivalent to 0.96 years of age-related LTL change
0.022
Further findings
Mechanisms linking BMI to LTL
- Increased low-grade systemic inflammation (circulating C-reactive protein) and lower circulating linoleic acid levels might link higher BMI to shorter LTL
Original publication
Investigating the impact of metabolic syndrome traits on telomere length: a Mendelian randomization study. Obesity (Silver Spring). Published 6 July 2023. doi:10.
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