Maternal alcohol binge-drinking in the first trimester and the risk of orofacial clefts in offspring: a large population-based pooling study

DeRoo, Lisa A.; Wilcox, Allen J.; Lie, Rolv Terje; Romitti, Paul A.; Pedersen, Dorthe; Munger, Ronald G.; Uribe, Lina M. Moreno; Wehby, George L.

doi:10.1007/s10654-016-0171-5

Cited by 42 publications

(31 citation statements)

References 35 publications

(31 reference statements)

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“…The model also adjusted for any maternal alcohol consumption and use of folic-acid-containing supplements in the first trimester, and age (≤18, 19–25, 26–30, 31–35, and ≥36 years), an indicator for low maternal education (incomplete high school versus higher education), and dummy variables representing the 6 contributing studies. These study-specific fixed effects account for differences among the study populations in oral cleft risk factors, prevalence, time effects, and case-to-control ratios (1, 3, 21). These fixed effects, as well as the balancing of cases and controls by year of birth within each study, ensured that time is not a confounder in the pooled analysis.…”

Section: Methodsmentioning

confidence: 99%

Interaction between smoking and body mass index and risk of oral clefts

Wehby

Uribe

Wilcox

et al. 2017

Annals of Epidemiology

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Purpose To examine maternal smoking and body mass index (BMI) interactions in contributing to risk of oral clefts. Methods We studied 4935 cases and 10,557 controls from 6 population-based studies and estimated a pooled logistic regression of individual-level data, controlling for study fixed effects and individual-level risk factors. Results We found a significant negative smoking-BMI interaction, with cleft risk with smoking generally declining with higher BMI. For all clefts combined, the OR for smoking was 1.61 (95% CI: 1.39–1.86) at BMI 17 (underweight), 1.47 (95% CI: 1.34–1.62) at BMI 22 (normal weight), 1.35 (95% CI: 1.22–1.48) at BMI 27 (overweight), 1.21 (95% CI: 1.04–1.41) at BMI 33 (obese), and 1.13 (95% CI: 0.92–1.38) at BMI 37 (very obese). A negative interaction was also observed for isolated clefts and across cleft types but was more pronounced for cleft lip only and cleft palate only. Conclusions Our findings suggest that the risk of oral clefts associated with maternal smoking is largest among underweight mothers, although the smoking-BMI interaction is strongest for cleft lip only and cleft palate only. BMI was not protective for the effects of smoking; a clinically relevant increase in smoking-related cleft risk was still present among heavier women.

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Section: Methodsmentioning

confidence: 99%

Interaction between smoking and body mass index and risk of oral clefts

Wehby

Uribe

Wilcox

et al. 2017

Annals of Epidemiology

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“…Evidence for maternal alcohol consumption as a risk factor is less consistent, although consuming large amounts over a short period of time (e.g. “binge drinking”) appears to increase risk 14 . Broad measures, e.g.…”

Section: Introductionmentioning

confidence: 99%

Genetic factors influencing risk to orofacial clefts: today’s challenges and tomorrow’s opportunities

2016

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Orofacial clefts include cleft lip (CL), cleft palate (CP), and cleft lip and palate (CLP), which combined represent the largest group of craniofacial malformations in humans with an overall prevalence of one per 1,000 live births. Each of these birth defects shows strong familial aggregation, suggesting a major genetic component to their etiology. Genetic studies of orofacial clefts extend back centuries, but it has proven difficult to define any single etiologic mechanism because many genes appear to influence risk. Both linkage and association studies have identified several genes influencing risk, but these differ across families and across populations. Genome-wide association studies have identified almost two dozen different genes achieving genome-wide significance, and there are broad classes of ‘causal genes’ for orofacial clefts: a few genes strongly associated with risk and possibly directly responsible for Mendelian syndromes which include orofacial clefts as a key phenotypic feature of the syndrome, and multiple genes with modest individual effects on risk but capable of disrupting normal craniofacial development under the right circumstances (which may include exposure to environmental risk factors). Genomic sequencing studies are now underway which will no doubt reveal additional genes/regions where variants (sequence and structural) can play a role in controlling risk to orofacial clefts. The real challenge to medicine and public health is twofold: to identify specific genes and other etiologic factors in families with affected members and then to devise effective interventions for these different biological mechanisms controlling risk to complex and heterogeneous birth defects such as orofacial clefts.

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“…2 According to some studies, alcohol consumption can inhibit retinoic acid production, increasing the risk of CL/P. 6,7 Smoking during pregnancy apparently doubles the risk of orofacial cleft in newborns. Moreover, in vitro studies have shown that tobacco inhibits palatal fusion and affects cell proliferation, leading to medial edge epithelial cell death.…”

Section: Introductionmentioning

confidence: 99%

Risk factors and comorbidities in Brazilian patients with orofacial clefts

et al. 2018

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Considering that environmental risk factors substantially contribute to the etiology of orofacial clefts and that knowledge about the characteristics and comorbidities associated with oral clefts is fundamental to promoting better quality of life, this study aimed to describe the risk factors, main characteristics, and comorbidities of a group of patients with cleft lip and/or cleft palate (CL/P) from Rio Grande do Norte (RN), Brazil. Data were obtained from 173 patients with CL/P using a form from the Brazilian database on Orofacial Clefts. Most patients were male with cleft lip and palate and had a normal size and weight at birth; presented few neonatal intercurrent events; and had anemia and respiratory and cardiovascular diseases as main associated comorbidities. They also required timely surgical rehabilitation and multidisciplinary care to stimulate their neuropsychomotor development. In addition, a high frequency of familial recurrence and of parental consanguinity was evidenced in the studied population, especially for the cleft lip and cleft palate type. Other relevant findings were the considerable maternal exposure to alcohol, infections, smoking, and hypertension, as well as low supplementation with vitamins and minerals and deliberate consumption of analgesics, antibiotics, and antihypertensives during pregnancy. Characterization of the CL/P patient profile is essential for the planning of health services and integration among the health professionals involved in the diagnosis and treatment of these malformations. Our results reinforce the need for additional research to confirm the association between environmental factors and the development of orofacial clefts.

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Maternal alcohol binge-drinking in the first trimester and the risk of orofacial clefts in offspring: a large population-based pooling study

Cited by 42 publications

References 35 publications

Interaction between smoking and body mass index and risk of oral clefts

Interaction between smoking and body mass index and risk of oral clefts

Genetic factors influencing risk to orofacial clefts: today’s challenges and tomorrow’s opportunities

Risk factors and comorbidities in Brazilian patients with orofacial clefts

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