Evidence map›Paper›PMID 38536799›Full record

ArticlePloS one2024

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

Maria E Bleil, Bradley M Appelhans, Steven E Gregorich, Robert A Hiatt, Glenn I Roisman, Cathryn Booth-LaForce

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Observational
  2. Article
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Maria E BleilChild, Family, & Population Health Nursing, University of Washington, Seattle, WA, United States of America.ORCID 0000-0002-2006-4533
Bradley M AppelhansDepartment of Preventive Medicine, Rush University Medical Center, Chicago, IL, United States of America.
Steven E GregorichDepartment of Medicine, University of California San Francisco, San Francisco, CA, United States of America.
Robert A HiattDepartment of Epidemiology & Biostatistics, University of California, San Francisco, San Francisco, CA, United States of America.
Glenn I RoismanInstitute of Child Development, University of Minnesota, Minneapolis, MN, United States of America.
Cathryn Booth-LaForceChild, Family, & Population Health Nursing, University of Washington, Seattle, WA, United States of America.

Funding

THE NICHD STUDY OF EARLY CHILD CARE--PHASE 3U10HD025447 · NICHD · UNIVERSITY OF WASHINGTON · PI BOOTH-LAFORCE, CATHRYN L · 1990 to 2007
$5.1M
Early Life Adversity and Adulthood Health: The Role of Pubertal DevelopmentR01HL130103 · NHLBI · UNIVERSITY OF WASHINGTON · PI BLEIL, MARIA E. · 2016 to 2020
$3.8M
Early Adversity, Childhood Educational Experiences, and Adulthood Physical HealthR01HD091132 · NICHD · UNIVERSITY OF WASHINGTON · PI BLEIL, MARIA E., ROISMAN, GLENN I · 2017 to 2022
$2.3M
NHLBI NIH HHS R01 HL130103NICHD NIH HHS R01 HD091132NICHD NIH HHS U10 HD025447
6 · The paper itself

Abstract

objectiveTo 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.

methodsSubjects 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.

resultsInspection 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).

conclusionFindings 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.

Indexed as

Cardiovascular DiseasesPubertyAdolescentAdultBody Mass IndexFemaleHumansLife Change EventsMenarche

Identifiers

PMID38536799
PMCPMC10971576

What Socratic holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.