title: Association of leukocyte telomere length with circulating biomarkers of the renin-angiotensin-aldosterone system: the Framingham Heart Study.
abstract: BACKGROUND
  Leukocyte telomere length (LTL) chronicles the cumulative burden of oxidative stress and inflammation over a life course. Activation of the renin-angiotensin-aldosterone system is associated with increased oxidative stress and inflammation. Therefore, LTL may be related to circulating biomarkers of the renin-angiotensin-aldosterone system.
  
  
  RESULTS
  We evaluated the cross-sectional relations of LTL (dependent variable) to circulating renin and aldosterone concentrations and the renin-to-aldosterone ratio (all logarithmically transformed; independent variables) in 1203 Framingham Study participants (mean age, 59 years; 51% women). We used multivariable linear regression and adjusted for age, blood pressure, hypertension treatment, smoking, diabetes mellitus, body mass index, hormone replacement therapy, serum creatinine, and the urine sodium-to-creatinine ratio. Overall, multivariable-adjusted LTL was inversely related to renin (beta coefficient per unit increase, -0.038; P=0.036), directly related to aldosterone (beta=0.099; P=0.002), and inversely related to the renin-to-aldosterone ratio (beta=-0.049; P=0.003). Relations of LTL to biomarkers were stronger in those with hypertension, although a formal test of interaction was not statistically significant (P=0.20). Individuals with hypertension displayed significant associations of LTL with renin (beta=-0.060; P=0.005), aldosterone (beta=0.134; P=0.002), and renin-to-aldosterone ratio (beta=-0.072; P<0.001). Participants with hypertension who were in the top tertile of the renin-to-aldosterone ratio had LTL that was 182 base pairs shorter relative to those in the lowest tertile.
  
  
  CONCLUSIONS
  In our community-based sample, LTL was shorter in individuals with a higher renin-to-aldosterone ratio, especially in participants with hypertension. Additional investigations are warranted to confirm our observations.
authors.affiliation: Framingham Heart Study of the National Heart, Lung, and Blood Institute, Framingham, MA 01702-5827, USA. vasan@bu.edu
authors.forename: Ramachandran S
authors.initials: RS
authors.lastname: Vasan
authors.forename: Serkalem
authors.initials: S
authors.lastname: Demissie
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kimura
authors.forename: L Adrienne
authors.initials: LA
authors.lastname: Cupples
authors.forename: Nader
authors.initials: N
authors.lastname: Rifai
authors.forename: Charles
authors.initials: C
authors.lastname: White
authors.forename: Thomas J
authors.initials: TJ
authors.lastname: Wang
authors.forename: Jeffrey P
authors.initials: JP
authors.lastname: Gardner
authors.forename: Xiaogian
authors.initials: X
authors.lastname: Cao
authors.forename: Emelia J
authors.initials: EJ
authors.lastname: Benjamin
authors.forename: Daniel
authors.initials: D
authors.lastname: Levy
authors.forename: Abraham
authors.initials: A
authors.lastname: Aviv
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002986:Clinical Trials as Topic; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012084:Renin-Angiotensin System / Q000502:physiology*; D016615:Telomere / Q000378:metabolism*
chemical_list: D015415:Biomarkers