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Impact of growth, gonadal hormones, adiposity and the sodium-to-potassium ratio on longitudinal adolescent measures of blood pressure at puberty

Abstract

Blood pressure (BP) rises rapidly at puberty. While this is partly due to normal development, factors like excess adiposity and a high intake of dietary sodium relative to potassium may contribute to a true increase in hypertension risk. This study aimed to assess the relative impact of growth, gonadal hormones, adiposity and the sodium-to-potassium ratio (Na:K) on longitudinal BP measures at puberty. This study analysed data from a three-year longitudinal cohort study of pubertal adolescents. Anthropometry, body composition (bio-electrical impedance), serum testosterone and oestradiol (mass spectrometry) were measured annually. Na:K was measured from three-monthly urine samples. These variables were used to predict annual BP measures using mixed modelling and ordinal regression. Data from 325 adolescents (11.7 ± 1.0 y; 55% male) were analysed, showing typical growth patterns at puberty. Systolic BP increased over time in both sexes (p < 0.01), with boys exhibiting a significantly steeper rise compared to girls. Adiposity variables (BMI z-score, percent body fat, fat mass, waist-to-height ratio) strongly and consistently predicted systolic and diastolic BP in both sexes (all p < 0.05). Systolic BP was also significantly and positively related to height (p < 0.05). No associations with BP were identified in either sex for gonadal hormones or Na:K. Similar results were obtained when BP was classified into hypertension categories. Relative to other developmental and diet-related variables tested, adiposity was found to be the strongest most consistent predictor of BP in pubertal adolescents. Findings highlight the importance of dedicated youth obesity management interventions and policy measures for reducing long-term hypertension and cardiovascular disease risks.

Australian New Zealand Clinical Trials Registry ACTRN12617000964314.

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Fig. 1: Longitudinal measures of blood pressure separated by sex.
Fig. 2: Longitudinal measures of urinary Na:K separated by sex.

Data availability

The datasets generated during and/or analysed during the current study are not publicly available but are available from the corresponding author on reasonable request.

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Acknowledgements

The authors thank the ARCHER study participants and their families, and research assistants Lisa Riley and Janet Symons. Thank you to the schools and communities of Central Western NSW that were key to the recruitment of this cohort.

Funding

The ARCHER study, including this secondary analysis, was supported by the National Health and Medical Research Council of Australia (GNT1003312 & GNT1165070), the Thyne Reid Foundation, the Children’s Hospital at Westmead Clinical School and Kids Research. Initial feasibility studies that led to the ARCHER study were supported by the Sydney Medical School Foundation and Australian Rotary Health.

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HLC, CJ, JW and KSS designed research; HLC and KSS conducted research; HLC and FLG analysed data and wrote paper; all authors interpreted data and critically reviewed manuscript; HLC had primary responsibility for final content; all authors read and approved the final manuscript.

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Correspondence to Hoi Lun Cheng.

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Cheng, H.L., Garden, F.L., Skilton, M.R. et al. Impact of growth, gonadal hormones, adiposity and the sodium-to-potassium ratio on longitudinal adolescent measures of blood pressure at puberty. J Hum Hypertens (2022). https://doi.org/10.1038/s41371-022-00774-x

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