Maternal Cigarette Smoking, Metabolic Gene Polymorphism, and Infant Birth Weight

Wang, Xiaobin; Zuckerman, Barry; Pearson, Colleen; Kaufman, Gary E.; Chen, Changzhong; Wang, Guoying; Niu, Tianhua; Wise, Paul H.; Bauchner, Howard; Xu, Xiping

doi:10.1001/jama.287.2.195

Cited by 527 publications

(284 citation statements)

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“…The initial recruitment and follow-up have been previously described. [46][47][48] This report included 105 Black children (59 males and 46 females), who were singleton, full-term births and whose cord blood and venous blood were collected at birth and within the first two years of life, respectively. Written informed consents were obtained from all participants in this study.…”

Section: Methodsmentioning

confidence: 99%

Individual variation and longitudinal pattern of genome-wide DNA methylation from birth to the first two years of life

et al. 2012

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Section: Methodsmentioning

confidence: 99%

Individual variation and longitudinal pattern of genome-wide DNA methylation from birth to the first two years of life

et al. 2012

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“…Further genetic polymorphisms in placental alkaline phosphatase in the fetus [54] and maternal genetic variation of the genes encoding the aromatic compound, inducible cytochrome P450, and glutathione S-transferase genes [55] have been associated with modifications of the effects of maternal smoking during pregnancy on birth weight of the offspring. Other maternal genetic polymorphisms that may influence maternal metabolism and are reported to be associated with size at birth include methylenetetrahydrofolate reductase [56] and G-protein beta 3 subunit [57].…”

Section: Fetal Genes and Size At Birthmentioning

confidence: 99%

Genetic Variations and Normal Fetal Growth

Petry¹,

Ong²

2006

Horm Res Paediatr

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Size at birth is said to be a highly heritable trait, with an estimated 30–70% of the variability a result of genetics. Data from family studies may be confounded, however, by potential interactions between fetal genes and the maternal uterine environment. Overall, the maternal environment tends to restrain fetal growth, and this is most evident in first pregnancies. Restraint of fetal growth appears to be inherited through the maternal line. Potential genetic candidates include the mitochondrial DNA 16189 variant, and common variants of exclusively maternally expressed genes, such as H19, which have been associated with size at birth. Maternal blood glucose levels and blood pressure are also correlated with size at birth, but the degree to which these changes relate to genetic variation in the mother is unclear. Elegant studies in mouse knockout models and rare genetic variants in humans have highlighted the importance of insulin-like growth factor I (IGF-I), IGF-II, insulin and their respective receptors in determining fetal growth. However, data linking common variation in the genes that regulate these proteins and receptors with size at birth are few and inconsistent. Interestingly, common variation in the insulin gene (INS) variable number tandem repeats, which regulates the transcription of insulin and IGF-II, has been associated with size at birth, largely in second and subsequent pregnancies, where maternal restraint is least evident. This suggests that fetal genes, and in particular paternally expressed genes, may have significant effects on fetal growth during pregnancies where maternal restraint of fetal growth is less evident.

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“…Nevertheless, the major role infectious processes may play in generating premature birth coupled with the evidence that these infections may be more prevalent in groups at high risk for preterm birth make the search for effective antibiotic therapy an arena of research of special relevance to the analysis of disparate infant outcomes (25). There is also recent evidence that genetic predispositions may mediate the impact of other environmental influences, such as maternal tobacco smoking, on prematurity (67). In this manner, genetic and other biologic insights are likely to help support rather than undermine the ultimate elucidation of social pathways of influence on disparate birth outcomes.…”

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The Anatomy of a Disparity in Infant Mortality

Wise

2003

Annu. Rev. Public Health

120

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This article suggests that while disparities in infant mortality have been longstanding, the mechanisms of disparity creation are undergoing intense change. This dynamic character is explored by first developing an analytic model that examines the interaction between social factors and the public health and clinical capacity to intervene. Disparities in infant mortality are then broken down into their component parts and linked to specific arenas of intervention. Disparities in postneonatal mortality are being shaped by differential access to interventions designed to prevent infant death from congenital anomalies and the Sudden Infant Death Syndrome. Disparities in neonatal mortality are primarily determined by factors that influence the birthrate of extremely premature infants and access to specialized obstetrical and pediatric care. This analysis suggests that the epidemiology and social meaning of disparities in infant mortality are intensely dynamic and increasingly reflect the interaction between social forces and technical innovation.

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Maternal Cigarette Smoking, Metabolic Gene Polymorphism, and Infant Birth Weight

Abstract: In our study, maternal CYP1A1 and GSTT1 genotypes modified the association between maternal cigarette smoking and infant birth weight, suggesting an interaction between metabolic genes and cigarette smoking.

Cited by 527 publications

References 34 publications

Individual variation and longitudinal pattern of genome-wide DNA methylation from birth to the first two years of life

Individual variation and longitudinal pattern of genome-wide DNA methylation from birth to the first two years of life

Genetic Variations and Normal Fetal Growth

The Anatomy of a Disparity in Infant Mortality

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