@article {Williams1849, author = {Dylan M Williams and Abigail Fraser and William D Fraser and Elina Hypp{\"o}nen and George Davey Smith and John Deanfield and Aroon Hingorani and Naveed Sattar and Debbie A Lawlor}, title = {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}, volume = {99}, number = {24}, pages = {1849--1856}, year = {2013}, doi = {10.1136/heartjnl-2013-303678}, publisher = {BMJ Publishing Group Ltd}, 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{\textendash}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.}, issn = {1355-6037}, URL = {https://heart.bmj.com/content/99/24/1849}, eprint = {https://heart.bmj.com/content/99/24/1849.full.pdf}, journal = {Heart} }