title: Reduced telomere length is not associated with early signs of vascular aging in young men born after intrauterine growth restriction: a paradox?
abstract: OBJECTIVE
  The mechanisms that increase cardiovascular risk in individuals born small for gestational age (SGA) are not well understood. Telomere shortening has been suggested to be a predictor of disease onset. Our aim was to determine whether impaired intrauterine growth is associated with early signs of vascular aging and whether telomere length could be a biomarker of this pathway.
  
  
  METHODS
  One hundred and fourteen healthy young men born SGA or after normal pregnancy [appropriate for gestational age (AGA)] were enrolled. Patient data were gathered from questionnaires and clinical exams, including blood pressure (BP) measurement routine laboratory analyses, and carotid intima-media thickness (cIMT). Leukocyte telomere length (LTL) was assessed by quantitative PCR. Birth data were obtained from medical records.
  
  
  RESULTS
  The SGA group had significantly higher pulse pressure and cIMT, and a trend to increased SBP and heart rate in comparison to the AGA group. Interestingly, SGA men exhibited a 42% longer LTL than the AGA group. LTL was inversely associated with age, BMI, BP and birth parameters. In multiple regression analysis, BMI was the key determinant of SBP and cIMT.
  
  
  CONCLUSIONS
  Young men born SGA show early signs of vascular aging. Unexpectedly, in our cohort, the SGA group had longer telomeres than the normal controls. Although longer telomeres are predictive of better health in the future, our findings could indicate a faster telomere attrition rate and probable early onset of cardiovascular risk in SGA participants. Follow-up of this cohort will clarify hypothesis and validate telomere dynamics as indicators of future health risks.
authors.affiliation: aDepartment for Nephrology, Hypertension, Dialysis and Transplantation, University Hospital Center Zagreb, Croatia bDanish Aging Research Center, University of Southern Denmark, Aarhus and Copenhagen, Denmark cDepartment for Molecular Biology, Ruđer Bošković Institute dDepartment of Cardiovascular Diseases, University Hospital Center eDepartment for Molecular Medicine, Ruđer Bošković Institute, Zagreb, Croatia fDepartment of Clinical Sciences, Lund University, Skåne University Hospital, Malmö, Sweden.
authors.forename: Mario
authors.initials: M
authors.lastname: Laganović
authors.forename: Laila
authors.initials: L
authors.lastname: Bendix
authors.forename: Ivica
authors.initials: I
authors.lastname: Rubelj
authors.forename: Majda Vrkić
authors.initials: MV
authors.lastname: Kirhmajer
authors.forename: Neda
authors.initials: N
authors.lastname: Slade
authors.forename: Ivana Vuković
authors.initials: IV
authors.lastname: Lela
authors.forename: Vedran
authors.initials: V
authors.lastname: Premužić
authors.forename: Peter M
authors.initials: PM
authors.lastname: Nilsson
authors.forename: Bojan
authors.initials: B
authors.lastname: Jelaković
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000209:etiology; D059168:Carotid Intima-Media Thickness; D016922:Cellular Senescence; D003430:Cross-Sectional Studies; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D006801:Humans; D007236:Infant, Small for Gestational Age; D016014:Linear Models; D008297:Male; D016615:Telomere; D055815:Young Adult