Genes as instruments for studying risk behavior effects: an application to maternal smoking and orofacial clefts

Wehby, George L.; Jugessur, Astanand; Murray, Jeffrey C.; Moreno, Lina M.; Wilcox, Allen J.; Lie, Rolv Terje

doi:10.1007/s10742-011-0071-9

Cited by 38 publications

(33 citation statements)

References 101 publications

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“…Other confounders such as maternal use of medications during pregnancy may also be at play. To further check for confounding, we estimated a model adding maternal smoking during pregnancy, a well-known risk factor for oral clefts and child development, as a covariate in addition to a dummy variable to indicate observations with missing data on smoking (∼40%) to retain the full sample 34 35. We found the same results as those in table 2 (see online supplementary table S1).…”

Section: Discussionmentioning

confidence: 63%

Children with oral clefts are at greater risk for persistent low achievement in school than classmates

et al. 2015

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Objectives To examine trajectories in academic achievement for children with oral clefts versus unaffected classmates and explore predictors of persistently low achievement among children with oral clefts. Design Longitudinal cohort study of academic achievement in a population-based sample. Setting and Participants Children born from 1983 through 2003 with oral clefts were identified from the Iowa Registry for Congenital and Inherited Disorders and matched to unaffected classmates by sex, school/school district, and month and year of birth. Main Outcome Measures Academic achievement was measured from Iowa Testing Programs (ITP) data. Outcomes included achievement scores in reading, language, and mathematics. Results Academic achievement data were available for 586 children with oral clefts and 1,873 unaffected classmates. Achievement trajectories were stable for both groups. Children with oral clefts were more likely than their classmates to be classified into persistent, low achievement trajectories, including when adjusting for socioeconomic differences: OR=1.63, 95% CI: 1.23–2.16 for reading; OR=1.73, 95% CI: 1.29–2.31 for language; OR=1.45, 95% CI: 1.05–1.99 for math. Predictors of low achievement were cleft palate only (versus other cleft types), adolescent mothers, low maternal education, and less frequent use of prenatal care. Conclusions Most children have steady academic trajectories and children with oral clefts are at greater risk for persistent, low achievement in school than unaffected classmates. These findings support the need for routine, early screening for academic deficits in this population. Cleft palate only, low parental education and adolescent mothers are associated with increased risk for persistent low achievement.

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Section: Discussionmentioning

confidence: 63%

Children with oral clefts are at greater risk for persistent low achievement in school than classmates

et al. 2015

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“…26,35 The pups exposed to nicotine had statistically significant LBW and shorter body length as compared to control group, confirming the momentous negative impact of maternal nicotine exposure on the size of the offspring. Additionally, frequency of stillborn pups was considerably higher in nicotine-treated dams, thus showing the deleterious effect of nicotine on the developing fetus.…”

Section: Discussionmentioning

confidence: 59%

“…25 Meanwhile, polymorphisms of several genes, including MSX1, TGFB3, BCL3, CYP1A1, GSTP1, and GSTT1 have been examined in conjunction with maternal alcohol consumption, cigarette smoking, medication use, and multivitamin supplementation during pregnancy. [25][26][27] It was shown that smoking by both parents interacts with a specific allelic variant of MSX1, which significantly increase the OFC risk for their offspring. 28 Moreover, a novel approach was developed by Wehby et al 26 to study the role of maternal smoking and OFC, in which they found out that smoking before and during pregnancy increased the risk of OFC by about 4-5 times at the sample average smoking rate.…”

Section: Discussionmentioning

confidence: 99%

“…[25][26][27] It was shown that smoking by both parents interacts with a specific allelic variant of MSX1, which significantly increase the OFC risk for their offspring. 28 Moreover, a novel approach was developed by Wehby et al 26 to study the role of maternal smoking and OFC, in which they found out that smoking before and during pregnancy increased the risk of OFC by about 4-5 times at the sample average smoking rate. Furthermore, in a recent genome-wide analysis study (GWAS), biases for maternally inherited genetic factors influencing the risk of OFC was suggested.…”

Section: Discussionmentioning

confidence: 99%

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Nicotine Exposure During Pregnancy Results in Persistent Midline Epithelial Seam With Improper Palatal Fusion

Öztürk

Sheldon

Sharma

et al. 2015

NICTOB

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Introduction: Nonsyndromic cleft palate is a common birth defect (1:700) with a complex etiology involving both genetic and environmental risk factors. Nicotine, a major teratogen present in tobacco products, was shown to cause alterations and delays in the developing fetus. Methods: To demonstrate the postpartum effects of nicotine on palatal development, we delivered three different doses of nicotine (1.5, 3.0, and 4.5 mg/kg/d) and sterile saline (control) into pregnant BALB/c mice throughout their entire pregnancy using subcutaneous micro-osmotic pump. Dams were allowed to deliver (~day 21 of pregnancy) and neonatal assessments (weight, length, nicotine levels) were conducted, and palatal tissues were harvested for morphological and molecular analyses, as well as transcriptional profiling using microarrays. Results: Consistent administration of nicotine caused developmental retardation, still birth, low birth weight, and significant palatal size and shape abnormality and persistent midline epithelial seam in the pups. Through microarray analysis, we detected that 6232 genes were up-regulated and 6310 genes were down-regulated in nicotine-treated groups compared to the control. Moreover, 46% of the cleft palate-causing genes were found to be affected by nicotine exposure. Alterations of a subset of differentially expressed genes were illustrated with hierarchal clustering and a series of formal pathway analyses were performed using the bioinformatics tools. Conclusions: We concluded that nicotine exposure during pregnancy interferes with normal growth and development of the fetus, as well results in persistent midline epithelial seam with type B and C patterns of palatal fusion. Implications: Although there are several studies analyzing the genetic and environmental causes of palatal deformities, this study primarily shows the morphological and large-scale genomic outcomes of gestational nicotine exposure in neonatal mice palate.

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“…These risk factors have been associated with a variety of adverse infant and child health outcomes and conditions including mortality, low birth weight (LBW), birth defects, asthma, obesity, and developmental delays/problems [1–4]. …”

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confidence: 99%

Candidate gene study for smoking, alcohol use, and body weight in a sample of pregnant women

Wehby¹,

Prater²,

Ryckman

et al. 2014

The Journal of Maternal-Fetal & Neonatal Medicine

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Objective Prenatal smoking, alcohol use, and obesity have significant effects on maternal and fetal health. However, not much is known about the genetic contributions to these risk factors among pregnant women. We evaluate the associations between several candidate genes and smoking, alcohol use, pre-pregnancy body weight, and weight gain during pregnancy in a sample of pregnant women. Methods The study analyzes a sample of about 1,900 mothers from the Danish National Birth Cohort. We test the association between 1,450 SNPs in/near 117 genes/loci and various risk factor measures. Results Only a few SNPs in FTO were significantly associated with pre-pregnancy obesity and body mass index (4 and 2 SNPs, respectively) after SNP-level correction for multiple testing. A few loci were significantly related to various smoking measures (any smoking, quitting, cigarette number) with gene/locus-level correction for multiple testing, but not after SNP-level correction. Similarly, some loci were significant for the alcohol measures at the gene/locus-level but not at SNP-level correction. Conclusion The study suggests that the majority of the evaluated candidate genes may not play an important role in influencing these risk factors among pregnant women, highlighting the importance of other genetic factors and non-genetic contributors to their etiology.

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Genes as instruments for studying risk behavior effects: an application to maternal smoking and orofacial clefts

Cited by 38 publications

References 101 publications

Children with oral clefts are at greater risk for persistent low achievement in school than classmates

Children with oral clefts are at greater risk for persistent low achievement in school than classmates

Nicotine Exposure During Pregnancy Results in Persistent Midline Epithelial Seam With Improper Palatal Fusion

Candidate gene study for smoking, alcohol use, and body weight in a sample of pregnant women

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