Lauren C Houghton1, Mandy Goldberg2, Ying Wei3, Piera M Cirillo4, Barbara A Cohn4, Karin B Michels5, Mary Beth Terry6. 1. Department of Epidemiology, Columbia University, Mailman School of Public Health, New York, NY. Electronic address: lh2746@columbia.edu. 2. Department of Epidemiology, Columbia University, Mailman School of Public Health, New York, NY. 3. Department of Biostatistics, Columbia University, Mailman School of Public Health, New York, NY. 4. The Center for Research on Women and Children's Health, The Child Health and Development Studies, Public Health Institute, Berkeley, CA. 5. Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, CA; Institute for Prevention and Cancer Epidemiology, Faculty of Medicine and Medical Center, University of Freiburg, Germany. 6. Department of Epidemiology, Columbia University, Mailman School of Public Health, New York, NY; Herbert Irving Comprehensive Cancer Center, Columbia Medical Center, New York, NY.
Abstract
PURPOSE: Studies suggests that intrauterine exposure to maternal smoking both accelerates or delays age at menarche. We hypothesize that these opposing findings relate to different infant and childhood growth patterns across cohorts. METHODS: Using data from an adult follow-up study of the Child Health and Development Studies and the National Collaborative Perinatal Project, we examined, using generalized estimating linear regression models, whether intrauterine exposure to maternal smoking was associated with age at menarche in 1090 daughters before and after accounting for growth in weight. RESULTS: Compared to the nonexposed, intrauterine exposure to maternal smoking was associated with a 4-month acceleration in menarche in the National Collaborative Perinatal Project (β = -0.35 years; 95% confidence interval [CI]: -0.63, -0.08), but a 6-month delay in menarche in the Child Health and Development Studies (β = 0.48 years; 95% CI: 0.13, 0.83), despite having a similar reduction in birth weight in both cohorts (∼300 g). The results were more consistent across cohorts when we stratified by postnatal growth patterns. For example, in those with rapid weight gain (increasing two growth references from 0 to 4 years), intrauterine exposure to maternal smoking was related to a 7-month acceleration in menarche (β = -0.56 years; 95% CI: -0.95, -0.17). CONCLUSIONS: These findings suggest that the association of intrauterine exposure to maternal smoking on age at menarche depends on postnatal growth patterns.
PURPOSE: Studies suggests that intrauterine exposure to maternal smoking both accelerates or delays age at menarche. We hypothesize that these opposing findings relate to different infant and childhood growth patterns across cohorts. METHODS: Using data from an adult follow-up study of the Child Health and Development Studies and the National Collaborative Perinatal Project, we examined, using generalized estimating linear regression models, whether intrauterine exposure to maternal smoking was associated with age at menarche in 1090 daughters before and after accounting for growth in weight. RESULTS: Compared to the nonexposed, intrauterine exposure to maternal smoking was associated with a 4-month acceleration in menarche in the National Collaborative Perinatal Project (β = -0.35 years; 95% confidence interval [CI]: -0.63, -0.08), but a 6-month delay in menarche in the Child Health and Development Studies (β = 0.48 years; 95% CI: 0.13, 0.83), despite having a similar reduction in birth weight in both cohorts (∼300 g). The results were more consistent across cohorts when we stratified by postnatal growth patterns. For example, in those with rapid weight gain (increasing two growth references from 0 to 4 years), intrauterine exposure to maternal smoking was related to a 7-month acceleration in menarche (β = -0.56 years; 95% CI: -0.95, -0.17). CONCLUSIONS: These findings suggest that the association of intrauterine exposure to maternal smoking on age at menarche depends on postnatal growth patterns.
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