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Associations of maternal 25-hydroxyvitamin D in pregnancy with offspring cardiovascular risk factors in childhood and adolescence: findings from the Avon Longitudinal Study of Parents and Children
  1. Dylan M Williams1,
  2. Abigail Fraser1,
  3. William D Fraser2,
  4. Elina Hyppönen3,
  5. George Davey Smith1,
  6. John Deanfield4,
  7. Aroon Hingorani5,
  8. Naveed Sattar6,
  9. Debbie A Lawlor1
  1. 1MRC Centre for Causal Analyses in Translational Epidemiology, School of Social and Community Medicine, University of Bristol, Bristol, UK
  2. 2Norwich Medical School, University of East Anglia, Norwich, UK
  3. 3Centre for Paediatric Epidemiology and Biostatistics, and Medical Research Council Centre of Epidemiology for Child Health, University College London Institute of Child Health, London, UK
  4. 4Institute of Child Health, University College London, London, UK
  5. 5Genetic Epidemiology Group, Department of Epidemiology and Public Health, University College London, London, UK
  6. 6BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK
  1. Correspondence to Professor Debbie Lawlor, School of Social and Community Medicine, University of Bristol, Oakfield House, Oakfield Grove, Bristol BS8 2BN, UK; d.a.lawlor{at}bristol.ac.uk

Abstract

Objective Lower maternal vitamin D status in pregnancy may be associated with increased offspring cardiovascular risk in later life, but evidence for this is scant. We examined associations of maternal total 25-hydroxyvitamin D (25(OH)D) in pregnancy with offspring cardiovascular risk factors assessed in childhood and adolescence.

Design A longitudinal, prospective study.

Setting The study was based on data from mother–offspring pairs in the Avon Longitudinal Study of Parents and Children (ALSPAC), a UK prospective population-based birth cohort (N=4109).

Outcome measures Offspring cardiovascular risk factors were measured in childhood (mean age 9.9 years) and in adolescence (mean age 15.4 years): blood pressure, lipids, apolipoproteins (at 9.9 years only), glucose and insulin (at 15.4 years only), C reactive protein (CRP), and interleukin 6 (at 9.9 years only) were measured.

Results After adjustments for potential confounders (maternal age, education, body mass index (BMI), smoking, physical activity, parity, socioeconomic position, ethnicity, and offspring gestational age at 25(OH)D sampling; gender, age, and BMI at outcome assessment), maternal 25(OH)D was inversely associated with systolic blood pressure (−0.48 mm Hg difference per 50 nmol/L increase in 25(OH)D; 95% CI −0.95 to −0.01), Apo-B (−0.01 mg/dL difference; 95% CI −0.02 to −0.001), and CRP (−6.1% difference; 95% CI −11.5% to −0.3%) at age 9.9 years. These associations were not present for risk factors measured at 15.4 years, with the exception of a weak inverse association with CRP (−5.5% difference; 95% CI −11.4% to 0.8%). There was no strong evidence of associations with offspring triglycerides, glucose or insulin.

Conclusions Our findings suggest that fetal exposure to 25(OH)D is unlikely to influence cardiovascular risk factors of individuals later in life.

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