TY - JOUR
T1 - Associations of maternal 25-hydroxyvitamin D in pregnancy with offspring cardiovascular risk factors in childhood and adolescence
T2 - Findings from the avon longitudinal study of parents and children
AU - Williams, Dylan M.
AU - Fraser, Abigail
AU - Fraser, William D.
AU - Hyppon̈en, Elina
AU - Smith, George Davey
AU - Deanfield, John
AU - Hingorani, Aroon
AU - Sattar, Naveed
AU - Lawlor, Debbie A.
PY - 2013/12
Y1 - 2013/12
N2 - 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 Parentsand 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 fi ndings suggest that fetal exposure to 25(OH)D is unlikely to influence cardiovascular risk factors of individuals later in life.
AB - 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 Parentsand 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 fi ndings suggest that fetal exposure to 25(OH)D is unlikely to influence cardiovascular risk factors of individuals later in life.
UR - http://www.scopus.com/inward/record.url?scp=84888025756&partnerID=8YFLogxK
U2 - 10.1136/heartjnl-2013-303678
DO - 10.1136/heartjnl-2013-303678
M3 - Article
C2 - 24125739
AN - SCOPUS:84888025756
SN - 1355-6037
VL - 99
SP - 1849
EP - 1856
JO - Heart
JF - Heart
IS - 24
ER -