Parental and offspring contribution of genetic markers of adult blood pressure in early life: The FAMILY study

• Published in: PloS one Vol. 12; no. 10; p. e0186218
• Main Authors: Robiou-du-Pont, Sébastien, Anand, Sonia S, Morrison, Katherine M, McDonald, Sarah D, Atkinson, Stephanie A, Teo, Koon K, Meyre, David
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 18.10.2017; Public Library of Science (PLoS)
• Subjects: Adult; Adults; Age; Arteriosclerosis; Atherosclerosis; Biology and Life Sciences; Blood; Blood pressure; Blood Pressure - genetics; Cardiovascular disease; Child, Preschool; Children; Children & youth; Epigenetics; Families & family life; Family studies; Female; Genealogy; Genetic aspects; Genetic effects; Genetic Markers; Genome-wide association studies; Genome-Wide Association Study; Genomes; Health sciences; Humans; Hypertension; Hypertension - genetics; Hypertension - physiopathology; Infant; Kinases; Loci; Male; Medical research; Medicine and Health Sciences; Methylenetetrahydrofolate reductase; Methylenetetrahydrofolate Reductase (NADPH2) - genetics; Mothers; Multiple births; Obesity; Offspring; Pediatrics; Physiological aspects; Polymorphism, Single Nucleotide; Proteins; Puberty; Research methodology; Risk Factors; Single-nucleotide polymorphism; Social Sciences; src-Family Kinases - genetics; Steroid 17-alpha-Hydroxylase - genetics; Studies; Teenagers; Canada; Ontario Canada
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0186218

Previous genome wide association studies (GWAS) identified associations of multiple common variants with diastolic and systolic blood pressure traits in adults. However, the contribution of these loci to variations of blood pressure in early life is unclear. We assessed the child and parental contributions of 33 GWAS single-nucleotide polymorphisms (SNPs) for blood pressure in 1,525 participants (515 children, 406 mothers and 237 fathers) of the Family Atherosclerosis Monitoring In early life (FAMILY) study followed-up for 5 years. Two genotype scores for systolic (29 SNPs) and diastolic (24 SNPs) blood pressure were built. Linear mixed-effect regressions showed significant association between rs1378942 in CSK and systolic blood pressure (β = 0.98±0.46, P = 3.4×10-2). The child genotype scores for diastolic and systolic blood pressure were not associated in children. Nominally significant parental genetic effects were found between the SNPs rs11191548 (CYP17A1) (paternal, β = 2.78±1.49, P = 6.1×10-2 for SBP and β = 3.60±1.24, P = 3.7×10-3 for DBP), rs17367504 (MTHFR) (paternal, β = 2.42±0.93, P = 9.3×10-3 for SBP and β = 1.89±0.80, P = 1.8×10-2 for DBP and maternal, β = -1.32±0.60, P = 2.9×10-2 and β = -1.97±0.77, P = 1.0×10-2, for SBP and DBP respectively) and child blood pressure. Our study supports the view that adult GWAS loci have a limited impact on blood pressure during the five first years of life. The parental genetic effects observed on blood pressure in children may suggest epigenetic mechanisms in the transmission of the risk of hypertension. Further replication is needed to confirm our results.