Abstract
BackgroundWhether earlier onset of puberty is associated with higher cardiovascular risk in early adulthood is not well understood. Our objective was to examine the association between puberty timing and markers of cardiovascular structure and function at age 25 years.MethodsWe conducted a prospective birth cohort study using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). Participants were born between April 1, 1991, and December 31, 1992. Exposure of interest was age at peak height velocity (aPHV), an objective and validated growth-based measure of puberty onset. Outcome measures included cardiovascular structure and function at age 25 years: carotid intima-media thickness (CIMT), left ventricular mass index (LVMI) and relative wall thickness (RWT), pulse wave velocity (PWV) and systolic blood pressure (SBP). Multiple imputation was used to impute missing data on covariates and outcomes. Linear regression was used to examine the association between aPHV and each measure of cardiac structure and function, adjusting for maternal age, gestational age, household social class, maternal education, mother’s partner’s education, breastfeeding, parity, birthweight, maternal body mass index, maternal marital status, maternal prenatal smoking status and height and fat mass at age 9. All analyses were stratified by sex.ResultsA total of 2752–4571 participants were included in the imputed analyses. A 1-year older aPHV was not strongly associated with markers of cardiac structure and function in males and females at 25 years and most results spanned the null value. In adjusted analyses, a 1-year older aPHV was associated with 0.003 mm (95% confidence interval (CI) 0.00001, 0.006) and 0.0008 mm (95% CI − 0.002, 0.003) higher CIMT; 0.02 m/s (95% CI − 0.05, 0.09) and 0.02 m/s (95% CI − 0.04, 0.09) higher PWV; and 0.003 mmHg (95% CI − 0.60, 0.60) and 0.13 mmHg (95% CI − 0.44, 0.70) higher SBP, among males and females, respectively. A 1-year older aPHV was associated with − 0.55 g/m2.7 (95% CI − 0.03, − 1.08) and − 0.89 g/m2.7 (95% CI − 0.45, − 1.34) lower LVMI and − 0.001 (95% CI − 0.006, 0.002) and − 0.002 (95% CI − 0.006, 0.002) lower RWT among males and females.ConclusionsEarlier puberty is unlikely to have a major impact on pre-clinical cardiovascular risk in early adulthood.
Highlights
Whether earlier onset of puberty is associated with higher cardiovascular risk in early adulthood is not well understood
The distribution/proportions of baseline characteristics by fourths of age at peak height velocity are shown in Table 1, and the characteristics of the cohort included in the analysis are shown in Additional file 1: Table S2
In confounder-adjusted analyses, a one-year older at peak height velocity (aPHV) was associated with 0.003 mm (95% confidence interval (CI) 0.00001, 0.006) higher carotid intima-media thickness, 0.02 m/s higher pulse wave velocity and 0.003 mmHg higher systolic blood pressure at 25 years
Summary
Whether earlier onset of puberty is associated with higher cardiovascular risk in early adulthood is not well understood. Our objective was to examine the association between puberty timing and markers of cardiovascular structure and function at age 25 years. Onset of puberty is a transitional period between childhood and adulthood with intense hormonal activity, including the release of gonadotropins, leptin, sex-steroids and growth hormone, leading to physical bodily changes and the appearance of secondary sexual characteristics. The most striking feature of puberty is a spurt in height which occurs in males in late puberty and is highly correlated with secondary sexual characteristics such as enlargement of larynx, deepening of voice and genitalia development [5]. Age at puberty onset has been decreasing for several decades, with increasing childhood adiposity (a condition of being severely overweight, or obese) thought to play a substantial role [10]
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