Abstract

BackgroundParents may play important roles in the regulation of children's weight status and consequently risk of childhood HTN. However, data relating parental dietary/lifestyle characteristics to risk of HTN in their children is sparse.ObjectiveUsing parental weight status as a marker of their dietary and lifestyle habits, we aimed to examine the association between parental weight status and risk of hypertension (HTN) in their children.MethodsA total of 1,949 children aged 6 to 12 years (1,012 girls) and their parents were enrolled. Information on demographics, anthropometrics, lifestyle, diet, and medical history were obtained from the participants and their parents through self‐administered questionnaires. Multivariable‐adjusted odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) of prevalent HTN in children in relation to parental weight status are presented.ResultsThe HTN prevalence in children was 8.4%, with no significant gender difference (9.0% in boys vs. 7.8% in girls, P=0.36). After adjusting for potential confounders, parental overweight was significantly associated with risk of HTN in children. Compared with children who had both parents being normal weight, the risk of childhood HTN was increased by 94% (OR=1.94; 95% CI: 1.08, 3.50) for children with only father being overweight and 109% (OR=2.09; 95% CI: 1.26, 3.46) for children with both parents being overweight. The observed association was attenuated after further adjustment for children's body mass index.ConclusionsFindings from this cross‐sectional study suggest that parental BMI levels were associated with higher prevalence of HTN in their children through the mediation of children's BMI. Because parental weight status is a marker of the dietary and lifestyle choices in a family, actions focusing on improving health awareness and changing unhealthy habits among parents may exert critical influence on the risk of childhood HTN.Support or Funding InformationThis work was partially supported by a grant from the NIH (R01ES021735).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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