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

Overview

Journal Heart

Date 2013 Oct 16

PMID 24125739

Citations 26

Authors

Dylan M Williams

Abigail Fraser

William D Fraser

Elina Hypponen

George Davey Smith

John Deanfield

Aroon Hingorani

Naveed Sattar

Debbie A Lawlor

Affiliations

Soon will be listed here.

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.

Citing Articles

Maternal vitamin D status in relation to cardiometabolic risk factors in children from the Norwegian Environmental Biobank.

Amberntsson A, Barebring L, Winkvist A, Lissner L, Brantsaeter A, Erlund I PLoS One. 2025; 20(2):e0318071.

PMID: 39999040 PMC: 11856322. DOI: 10.1371/journal.pone.0318071.

Inflammation proteomics datasets in the ALSPAC cohort.

Goulding N, Goudswaard L, Hughes D, Corbin L, Groom A, Ring S Wellcome Open Res. 2024; 7:277.

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Amaro-Gahete F, Vazquez-Lorente H, Jurado-Fasoli L, Dote-Montero M, Kohler I, Ruiz J J Endocrinol Invest. 2024; 47(7):1645-1656.

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The Epigenetic Legacy of Maternal Protein Restriction: Renal DNA Methylation Changes in Hypertensive Rat Offspring.

Jia H, Miyoshi M, Li X, Furukawa K, Otani L, Shirahige K Nutrients. 2023; 15(18).

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The Impact of Nutrient Intake and Metabolic Wastes during Pregnancy on Offspring Hypertension: Challenges and Future Opportunities.

Tain Y, Hsu C Metabolites. 2023; 13(3).

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