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. 2024 Mar 27;19(3):e0299433.
doi: 10.1371/journal.pone.0299433. eCollection 2024.

Pubertal timing: A life course pathway linking early life risk to adulthood cardiometabolic health

Maria E Bleil  1 , Bradley M Appelhans  2 , Steven E Gregorich  3 , Robert A Hiatt  4 , Glenn I Roisman  5 , Cathryn Booth-LaForce  1
Affiliations

Pubertal timing: A life course pathway linking early life risk to adulthood cardiometabolic health

Maria E Bleil et al. PLoS One. .

Abstract

Objective: To evaluate a series of prospective life course models testing whether the timing of pubertal development is a pathway through which prepubertal risk factors may influence adulthood cardiometabolic health.

Methods: Subjects were 655 female participants in the NICHD Study of Early Child Care and Youth Development (SECCYD) and recent SECCYD 30-year follow-up, the Study of Health in Early and Adult Life (SHINE). Prepubertal risk factors included maternal menarcheal age, child race/ethnicity, child health status indicators, and child adversity indicators. Pubertal timing was indexed by breast development onset (Tanner stage [TS] II), pubic hair onset (TS II) and menarcheal age. Adulthood cardiometabolic risk (CMR) was indexed by a composite of waist circumference, systolic blood pressure, diastolic blood pressure, hemoglobin A1c, C-reactive protein, and high-density lipoprotein.

Results: Inspection of paths between the prepubertal risk factors, pubertal timing indicators, and adulthood CMR composite showed later breast development onset (-0.173, p < .01), later pubic hair onset (-0.182, p < .01), and later menarche (-0.145, p < .01) each predicted lower adulthood CMR, and each pubertal timing indicator mediated effects of prepubertal risk factors on adulthood CMR. Specifically, the timing of breast development onset and menarche mediated effects of maternal menarcheal age, Black (vs. White), Asian/PI (vs. White), child BMI percentile, and child SES on adulthood CMR (all ps < .05), and the timing of pubic hair onset mediated effects of maternal menarcheal age, Black (vs. White), and child BMI percentile on adulthood CMR (all ps < .10).

Conclusion: Findings in the current study contribute to the broader literature by identifying pubertal development and its timing as a potentially important pathway through which early life exposures may shape adulthood cardiometabolic health and disease. These findings have important implications for novel opportunities for increased surveillance and potential intervention focusing on pubertal development as a target to improve health more broadly.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Fig 1
Fig 1. Reported from adjusted models, the solid arrows represent direct effects (with p-values < .10) between the prepubertal risk factors and age at breast development onset (TS II) as well as age at breast development onset (TS II) and the adulthood CMR composite.
The dotted arrows represent the indirect (mediated) effects of these prepubertal risk factors on the adulthood CMR composite via age at breast development onset (TS II). Results suggest earlier pubertal onset, marked by the initiation of breast development, is a pathway through which risk for poor cardiometabolic health in adulthood is transmitted both directly and indirectly. *Direct effects (not depicted) were also observed for child BMI percentile (0.006, p < .01), childhood SES (-0.153, p < .05), and maternal sensitivity (-0.131, p = .080) predicting the adulthood CMR composite.
Fig 2
Fig 2. Reported from adjusted models, the solid arrows represent direct effects (with p-values < .10) between the prepubertal risk factors and age at pubic hair onset (TS II) as well as age at pubic hair onset (TS II) and the adulthood CMR composite.
The dotted arrows represent the indirect (mediated) effects of these prepubertal risk factors on the adulthood CMR composite via age at pubic hair onset (TS II). Results suggest earlier pubertal onset, marked by the initiation of pubic hair, is a pathway through which risk for poor cardiometabolic health in adulthood is transmitted both directly and indirectly. *Direct effects (not depicted) were also observed for child BMI percentile (0.007, p < .001), child SES (-0.167, p < .05), and maternal sensitivity (-0.126, p = .074) predicting the adulthood CMR composite.
Fig 3
Fig 3. Reported from adjusted models, the solid arrows represent direct effects (with p-values < .10) between the prepubertal risk factors and menarcheal age as well as menarcheal age and the adulthood CMR composite.
The dotted arrows represent the indirect (mediated) effects of these prepubertal risk factors on the adulthood CMR composite via menarcheal age. Results suggest earlier pubertal onset, marked by menarcheal age, is a pathway through which risk for poor cardiometabolic health in adulthood is transmitted both directly and indirectly. *Direct effects (not depicted) were also observed for child BMI percentile (0.006, p < .01) and child SES (-0.141, p = .076) predicting the adulthood CMR composite.
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