Literature DB >> 25740885

Prenatal smoking and age at menarche: influence of the prenatal environment on the timing of puberty.

A M Behie1, M H O'Donnell2.   

Abstract

STUDY QUESTION: Do prenatal exposure to cigarette smoking and birthweight influence age at menarche (AAM) in a cohort of Australian girls? SUMMARY ANSWER: We find that prenatal smoke exposure and lower birthweight increase the chance of earlier menarche in accordance with theoretical predictions as do confounding factors of maternal AAM and higher BMI of the girls. WHAT IS KNOWN ALREADY: Much prior research focuses on the role of the early childhood environment in determining AAM but fewer studies consider the role of the prenatal environment. Those studies that examine the prenatal period find an acceleration of maturation associated with maternal smoking and low birthweight. Life history theory predicts that early life exposure to stressful environments should promote more rapid maturation and that this timing can be established before birth, making the prenatal environment particularly important. STUDY DESIGN, SIZE, DURATION: Statistical analysis of longitudinal survey data collected from a large cohort (n = 2446) of Australian children using data from birth to 12-13 years of age. PARTICIPANTS/MATERIALS, SETTING,
METHODS: Owing to missing data, 1493 girls were included in the final analysis. Using cox regression, we examine how (i) maternal cigarette smoking during gestation and (ii) birthweight influence girls' AAM. Cox regression was used because not all girls had reached menarche. MAIN RESULTS AND THE ROLE OF CHANCE: We find that older maternal AAM (hazards ratio (HR): 0.75, confidence interval (CI) (95%): 0.71-0.79) and higher birthweight (HR: 0.86, CI (95%): 0.75-0.97) lower the chance of earlier menarche; while higher girls' BMI at 8-9 years (HR: 1.12, CI (95%): 1.10-1.15), and maternal cigarette smoking on 'most days' during gestation (HR: 1.40, CI (95%): 1.10-1.79 with 'no smoking' as the reference level) increased the chance of earlier menarche. All factors were statistically significant at P = 0.05. LIMITATIONS, REASONS FOR CAUTION: Not all girls had reached menarche, necessitating the use of cox regression. As with other longitudinal studies, there was study sample attrition and some missing data, particularly in reports of maternal smoking. In addition, as the degree of bias in the missing data is unknown, possible inaccurate reporting of maternal smoking may influence the results of birthweight on AAM. WIDER IMPLICATIONS OF THE
FINDINGS: Because of the association between younger AAM and higher risk of uterine, endometrial and breast cancer development, our finding adds to the need to consider the stress caused by prenatal smoke exposure as an important health risk. In addition, this study needs to be extended, when the same girls are 14-15 years of age, and on a larger dataset from a younger cohort within the same Australian Government project. STUDY FUNDING/COMPETING INTERESTS: No funding was received for this study and there are no competing interests to declare.
© The Author 2015. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Entities:  

Keywords:  birthweight; menarche; prenatal exposure delayed effects; sexual maturation; smoking

Mesh:

Substances:

Year:  2015        PMID: 25740885     DOI: 10.1093/humrep/dev033

Source DB:  PubMed          Journal:  Hum Reprod        ISSN: 0268-1161            Impact factor:   6.918


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