Association of pre- and post-natal parental smoking with offspring body mass index: An 8-year follow-up of a birth cohort
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany. Pediatric Obesity
(Impact Factor: 4.57).
02/2013; 9(2). DOI: 10.1111/j.2047-6310.2012.00146.x
Although many epidemiological studies have shown an association between maternal smoking during pregnancy and offspring overweight, it is still under debate whether intrauterine tobacco smoke exposure directly affects offspring obesity or if the association is rather due to confounding by lifestyle factors. The association of parental smoking habits at pre- and post-natal periods with offspring body mass index (BMI) was investigated, whereas maternal smoking during pregnancy was validated by cord serum cotinine measurements. Multivariable linear regression analysis, based on the German Ulm Birth Cohort Study of 1045 children born in 2000 with annual/biennial follow-up until the age of 8 years (n = 609), was conducted. BMI of offspring from mothers who smoked during pregnancy and non-smoking mothers differed significantly at 8 years. Maternal smoking during pregnancy was associated with an increase in BMI of 0.73 kg m−2 [95% confidence interval: 0.21–1.25] in 8-year-old children after adjustment for multiple potential confounding variables. Both pre- and post-natal smoking of fathers (0.34 [0.01–0.66]/0.45 [0.08–0.81]) and of both parents (1.03 [0.43–1.63]/0.56 [0.14–0.98]) were likewise significantly associated with offspring BMI. The observed patterns suggest that residual confounding by living conditions in smoking families rather than specific intrauterine exposure to tobacco smoke may account for the increased risk of offspring overweight.
Available from: Christina Sobotzki (born Riedel)
- "At lower quantiles the association was more pronounced in girls than in boys, whereas for higher quantiles the association was more pronounced and increased to a greater extent over time in boys compared with girls. Some previous studies have compared BMI or BMI z-scores in cohorts of children of smoking and nonsmoking mothers in repetitive cross-sectional analyses (Florath et al. 2013; Fried et al. 1999; Power and Jefferis 2002; Vik et al. 1996). The time period varied from birth to 33 years of age, although not all studies considered the life course since birth (Power and Jefferis 2002). "
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ABSTRACT: Offspring of smoking mothers during pregnancy have a lower birth weight but have a higher chance to become overweight during childhood.
We followed children longitudinally to assess the age when higher BMI z-scores became evident in the children of mothers who smoked during pregnancy, and evaluate the trajectory of changes until adolescence.
We pooled data from two German cohort studies that included repeated anthropometric measurements until 14 years and information on smoking during pregnancy and other risk factors for overweight. We used longitudinal quantile regression to estimate age- and sex-specific associations between maternal smoking and the 10(th), 25(th), 50(th), 75(th), and 90(th) quantiles of the BMI z-score distribution in study participants from birth through 14 years of age, adjusted for potential confounders. We used additive mixed models to estimate associations with mean BMI z-scores.
Mean and median (50(th) quantile) BMI z-scores at birth were smaller in the children of mothers who smoked during pregnancy compared with children of nonsmoking mothers, but BMI z-scores were significantly associated with maternal smoking beginning at the age of 4-5 years, and differences increased over time. For example, the difference in the median BMI z-score between the daughters of smokers versus nonsmokers was 0.12 (95% CI: 0.01, 0.21) at 5 years, and 0.30 (95% CI: 0.08, 0.39) at 14 years of age. For lower BMI z-score quantiles the association with smoking was more pronounced in girls, whereas in boys the association was more pronounced for higher BMI z-score quantiles.
A clear difference in BMI z-score (mean and median) between offspring of smoking and nonsmoking mothers emerged at the age of 4 to 5 years. The shape and size of age-specific effect estimates for maternal smoking during pregnancy varied by age and gender across the BMI z-score distribution.
Available from: hmg.oxfordjournals.org
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ABSTRACT: Understanding the role of epigenetic modifications, e.g. DNA methylation, in the process of aging requires the characterization of methylation patterns in large cohorts. We analysed > 480 000 CpG sites using Infinium HumanMethylation450 BeadChip (Illumina) in whole blood DNA of 965 participants of a population-based cohort study aged between 50 and 75 years. In an exploratory analysis in 400 individuals, 200 CpG sites with the highest Spearman correlation coefficients for the association between methylation and age were identified. Of these 200 CpGs, 162 were significantly associated with age, which was verified in an independent cohort of 498 individuals using mixed linear regression models adjusted for gender, smoking behaviour, age-related diseases and random batch effect and corrected for multiple testing by Bonferroni. In another independent cohort of 67 individuals without history of major age-related diseases and with a follow-up of 8 years, we observed a gain in methylation at 96% (52%, significant) of the positively age-associated CpGs and a loss at all (89%, significant) of the negatively age-associated CpGs in each individual while getting 8 years older. A regression model for age prediction based on 17 CpGs as predicting variables explained 71% of the variance in age with an average accuracy of 2.6 years. In comparison with cord blood samples obtained from the Ulm Birth Cohort Study, we observed a more than 2-fold change in mean methylation levels from birth to older age at 86 CpGs. We were able to identify 65 novel CpG sites with significant association of methylation with age. © The Author 2013. Published by Oxford University Press. All rights reserved. For Permissions, please email: [email protected]
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ABSTRACT: Lower respiratory tract infections (LRTIs) are a major cause of hospitalization in infants. Research suggests that immunomodulatory properties of vitamin D may influence LRTI risk. This study's objective was to examine whether 25-hydroxyvitamin D [25(OH)D] concentrations in cord blood influenced susceptibility to LRTI in the first year of life. Data was analyzed from a prospective birth cohort of 777 mother-infant pairs based in Ulm, Germany. Relative risks (RRs) of LRTI in relation to 25(OH)D cord blood levels were estimated by log-binomial regression after adjustment for potential confounders. To account for seasonal variation in both vitamin D levels and infections, we examined the association in different seasons. Analyses were conducted using clinical predefined cutpoints, quartiles, and season-standardized 25(OH)D quartiles. We observed a statistically significant association between 25(OH)D status in cord blood and risk of LRTI across the year using clinical cutpoints. The adjusted RR of LRTI for individuals with vitamin D deficiency (<25 nmol/L) in comparison to the referent category (>50 nmol/L) was 1.32 [95 % confidence interval (CI) 1.00, 1.73]. The association differed by maternal allergy status; children born to mothers without allergy demonstrated a RR of 1.45 (95 % CI 1.03, 2.03). The effect was largely driven by a strong association between 25(OH)D and LRTI in infants born in fall with a RR of 3.07 (95 % CI 1.37, 6.87). Our findings suggest that vitamin D deficiency at birth is associated with increased risk of LRTI particularly in infants born to mothers without allergy. The association seems strongest in infants born in fall.
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