Objective To examine independent associations of serum 25-hydroxyvitamin D (25(OH)D), parathyroid hormone (PTH) and calcium with a range of cardiovascular risk factors in adolescents.
Design Cross-sectional population-based study.
Setting A nationally representative sample of the US adolescent population.
Participants Healthy adolescents (aged 12–19) participating in the National Health and Nutrition Examination Survey (NHANES) between 2001 and 2006. Numbers varied between 740 and 5609 for given exposure and outcome associations.
Main outcome measures Systolic blood pressure (SBP), diastolic blood pressure (DBP), lipids (triglycerides, low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)), fasting insulin and glucose, postload glucose and glycohaemoglobin (HbA1c).
Results 25(OH)D was inversely associated with SBP (−0.068 standard deviations (SD), 95% CI −0.118 to −0.018), and positively associated with HDL-C (0.101; 0.040 to 0.162) and HbA1c (0.073; 0.021 to 0.125) after adjustment for gender, age, ethnicity, socioeconomic status and waist circumference. In adjusted models, PTH was inversely associated with triglycerides (−0.115; −0.188 to −0.042) and LDL-C (−0.133; −0.207 to −0.060). In adjusted models, calcium was positively associated with fasting insulin (0.110; 0.060 to 0.160), postload glucose (0.116; 0.000 to 0.232), HbA1c (0.079; 0.035 to 0.123), triglycerides (0.182; 0.122 to 0.242), HDL-C (0.049; 0.010 to 0.088) and LDL-C (0.137; 0.080 to 0.195). The associations of each exposure with risk factors remained after mutual adjustment for each other.
Conclusion Higher calcium levels might be a more important predictor of increased cardiovascular risk in adolescents than lower 25(OH)D levels or PTH levels, but the findings require replication in additional studies and examination in prospective studies.
- Vitamin D
- parathyroid hormone
- paediatric cardiology
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Funding UK Medical Research Council (MRC). 20 Park Crescent, London, W1B 1AL, UK. Other Funders: Wellcome Trust. Work on this study is funded by an UK MRC Grant (G0701603). The UK Medical Research Council (MRC) (G0600705) and the University of Bristol provide core funding for the UK MRC Centre of Causal Analyses in Translational Epidemiology, where all authors work. AF is funded by a UK MRC research fellowship. DW is funded by a Wellcome Trust 4-year PhD studentship in molecular, genetic and lifecourse epidemiology [WT083431MA].
Competing interests None.
Ethics approval This study was conducted with the approval of the Part of NHANES protocol.
Provenance and peer review Not commissioned; externally peer reviewed.
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