Maternal caffeine consumption and risk of neural tube defects

Department of Psychiatry, University of California Davis Medical Center, University of California, Davis, CA, USA.
Birth Defects Research Part A Clinical and Molecular Teratology (Impact Factor: 2.09). 11/2009; 85(11):879-89. DOI: 10.1002/bdra.20624
Source: PubMed


Animal studies demonstrate teratogenic effects of caffeine, whereas human studies are inconclusive.
Associations between maternal caffeine consumption and neural tube defects (NTDs) by type of NTD (anencephaly, spina bifida, or encephalocele) were examined using data from the National Birth Defects Prevention Study (NBDPS). Total average daily caffeine from coffee, tea, soda, and chocolate consumption during the year before pregnancy was estimated for 768 mothers of infants with NTDs and 4143 mothers of infants without birth defects who gave birth during 1997 through 2002. Periconceptional use of caffeine-containing medications was evaluated separately. Adjusted odds ratios (OR) and 95% confidence intervals (CI) associated with consumption of total caffeine and each caffeine source were estimated from logistic regression models.
Positive associations were observed between spina bifida and total caffeine consumption (OR 1.4; 95% CI: 1.1-1.9) and each caffeine source except caffeinated tea, which showed a negative association with spina bifida (OR 0.7; 95% CI: 0.6-0.9). Associations with modestly increased risk of NTDs and encephalocele were also observed. The association between caffeine consumption and anencephaly differed by maternal race/ethnicity. No dose effects were found.
Additional studies should confirm whether women who consume caffeine are at increased risk for pregnancies complicated by NTDs.

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Available from: Charlotte Druschel, May 09, 2014
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    • "Studies have demonstrated a link between caffeine consumption and neural tube defects (NTD) [12], [13]. To further investigate this matter, we administered different concentrations of caffeine into in vivo chick embryos as shown in Fig. 1A. "
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    ABSTRACT: Caffeine consumption is worldwide. It has been part of our diet for many centuries; indwelled in our foods, drinks, and medicines. It is often perceived as a "legal drug", and though it is known to have detrimental effects on our health, more specifically, disrupt the normal fetal development following excessive maternal intake, much ambiguity still surrounds the precise mechanisms and consequences of caffeine-induced toxicity. Here, we employed early chick embryos as a developmental model to assess the effects of caffeine on the development of the fetal nervous system. We found that administration of caffeine led to defective neural tube closures and expression of several abnormal morphological phenotypes, which included thickening of the cephalic mesenchymal tissues and scattering of somites. Immunocytochemistry of caffeine-treated embryos using neural crest cell markers also demonstrated uncharacteristic features; HNK1 labeled migratory crest cells exhibited an incontinuous dorsal-ventral migration trajectory, though Pax7 positive cells of the caffeine-treated groups were comparatively similar to the control. Furthermore, the number of neurons expressing neurofilament and the degree of neuronal branching were both significantly reduced following caffeine administration. The extent of these effects was dose-dependent. In conclusion, caffeine exposure can result in malformations of the neural tube and induce other teratogenic effects on neurodevelopment, although the exact mechanism of these effects requires further investigation.
    PLoS ONE 08/2012; 7(3):e34278. DOI:10.1371/journal.pone.0034278 · 3.23 Impact Factor
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    • "In case of coffee intake frequency, the pre-pregnancy coffee intake ratio was significantly higher in HS group (P < 0.01). In the study on the risk for neural tube damage in pregnant women and their infants with caffeine intake [16], the risk for spina bifida in infants was increased in the group of pregnant women who had more than 10 mg/day caffeine through coffee, tea, soda beverages or chocolate before pregnancy. Thus it is noticeable that pre-pregnancy lifestyle of pregnant women can influence the emotional state of pregnant women and lead to undesirable pregnancy outcomes. "
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    ABSTRACT: The aim of this study was to analyse effects that the degree of depression have on the life style variables, nutrient intake, iron indices and pregnancy outcome. Subjects were 114 pregnant women who were receiving prenatal care at a hospital in Seoul. We collected data for general characteristics and lifestyle variables from general survey instrument and for depression score from the questionnaire on depression. Dietary intakes of subjects were estimated by 24 hour dietary recall method. Also we analysed iron indices and pregnancy outcomes. We classified subjects by 10 point, which was the average depression score, into two groups [Low depression score group (LS) : High depression score group (HS)]. As to the intakes of total calcium, plant-calcium, plant-iron, potassium, total folate and dietary folate, LS group was far higher than HS group (P < 0.05, P < 0.05, P < 0.01, P < 0.001, P < 0.05, and P < 0.01, respectively). As to pre-pregnancy alcohol drinking, LS group had 41.9% in non-drinker, which was far higher than 28% in HS group in non-drinker (P < 0.05). As for drinking coffee during pre-pregnancy, pregnant women who don't drink coffee in LS group took 43.6%, which was higher than 38% in HS group (P < 0.01). Regarding delivery type, the cesarean section in LS group (18%) was significantly lower than that in HS group (45%) (P < 0.01). Bivariate analysis showed that birth weight was significantly associated with the gestational age (P < 0.01). The pregnant women with higher depression score tended to have undesirable life habit, which might affect negative pregnancy outcomes. A better understanding of how depression and intake of nutrients work together to modulate behavior will be benefit nutritional research.
    Nutrition research and practice 08/2010; 4(4):323-31. DOI:10.4162/nrp.2010.4.4.323 · 1.44 Impact Factor
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    • "The validity and reliability of caffeine assessment are high for the Willett food frequency questionnaire on which the food frequency for the current study was based (Munger et al., 1992), and classification of 'any' versus 'none' used for this study are likely more accurate than for the amount. However, information on caffeinated beverage intake was not specific to the time of neural tube closure and misclassification of caffeine intake during this time was possible, and probably at least partially explains the lack of a dose effect described previously (Schmidt et al., 2009). For caffeinated coffee, tea, and soda, we knew whether mothers consumed more, less, the same, or none during pregnancy, but not when they changed their intake or what their intake levels were during pregnancy. "
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    ABSTRACT: Investigations of maternal caffeine intake and neural tube defects (NTDs) have not considered genetic influences. Caffeine metabolism gene effects were examined in the National Birth Defects Prevention Study. Average daily caffeine was summed from self-reported coffee, tea, soda, and chocolate intake for mothers of 768 NTD cases, and 4143 controls delivered from 1997 to 2002. A subset of 306 NTD and 669 control infants and their parents were genotyped for CYP1A2*1F, NAT2 481C>T, and NAT2 590G>A. CYP1A2*1F was classified by fast or slow oxidation status, and NAT2 variants were categorized into rapid or slow acetylation status. Case-control logistic regression analyses, family-based transmission/disequilibrium tests and log-linear analyses, and hybrid log-linear analyses were conducted to produce odds ratios (ORs) or relative risks (RRs) and 95% confidence intervals (CIs) for caffeine intake and maternal and infant gene variants, and to examine interaction effects. NTDs were independently associated with infant slow NAT2 acetylator status (RR, 2.00; 95% CI, 1.10-3.64) and maternal CYP1A2*1F fast oxidation status (OR, 1.49; 95% CI, 1.10-2.03). Mothers who consumed caffeine, oxidized CYP1A2*1F quickly, and acetylized NAT2 slowly had a nonsignificantly elevated estimated risk for an NTD-affected pregnancy (OR, 3.10; 95% CI, 0.86-11.21). Multiplicative interaction effects were observed between maternal caffeine and infant CYP1A2*1F fast oxidizer status (p(interaction) = 0.03). The association identified between maternal CYP1A2*1F fast oxidation status and NTDs should be examined further in the context of the other substrates of CYP1A2. Maternal caffeine and its metabolites may be associated with increased risk for NTD-affected pregnancies in genetically susceptible subgroups.
    Birth Defects Research Part A Clinical and Molecular Teratology 07/2010; 88(7):560-9. DOI:10.1002/bdra.20681 · 2.09 Impact Factor
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