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Maternal, but not paternal or grandparental, caffeine intake is associated with childhood obesity and adiposity: The Lifeways Cross-Generation Cohort Study.

ABSTRACT: BACKGROUND:Maternal caffeine intake is associated with adverse birth outcomes, but its long-term influence on offspring adiposity outcomes is not well studied. Furthermore, few studies have investigated paternal and grandparental caffeine intake in relation to offspring outcomes. OBJECTIVE:To study the associations between maternal, paternal, and grandparental caffeine intake and offspring childhood adiposity. DESIGN:The core study sample consists of 558 mother-child pairs from the Lifeways Study. Caffeine intake was derived from relevant food items in a self-administered validated food frequency questionnaire in early pregnancy. Children's body mass index (BMI) and waist circumference (WC) were measured at 5- and 9-y follow-up. Childhood overall and central obesity were defined as age- and sex-specific BMI z-score > International Obesity Task Force cut-off and WC z-score > 90th percentile, respectively. Multiple linear and logistic regressions were used to assess associations. RESULTS:Study mothers had a mean age of 30.8 y and a mean prepregnancy BMI (kg/m2) of 23.7. In adjusted models, maternal caffeine intake was associated with a higher offspring BMI z-score [? (95% CI): 0.13 (0.06, 0.21) for year 5 and 0.17 (0.04, 0.29) for year 9; per 100 mg/d increment in maternal caffeine intake], WC z-score [? (95% CI): 0.09 (0.01, 0.17) for year 5 and 0.19 (0.05, 0.32) for year 9], and a higher risk of offspring overall obesity [OR (95% CI): 1.32 (1.11, 1.57) for year 5 and 1.44 (1.10, 1.88) for year 9] and central obesity [1.28 (1.02, 1.60) for year 5 and 1.62 (1.12, 2.34) for year 9]. The influence was stronger for coffee caffeine than tea caffeine. No consistent associations were observed for paternal and grandparental caffeine intake. CONCLUSIONS:Maternal antenatal, but not paternal or grandparental, caffeine intake is associated with higher offspring adiposity and obesity risk at age 5 and 9 y, with stronger associations observed for coffee caffeine. This prospective observational study was registered at the ISRCTN Registry as ISRCTN16537904.

SUBMITTER: Chen LW

PROVIDER: S-EPMC7484488 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Maternal, but not paternal or grandparental, caffeine intake is associated with childhood obesity and adiposity: The Lifeways Cross-Generation Cohort Study.

Chen Ling-Wei LW Murrin Celine M CM Mehegan John J Kelleher Cecily C CC Phillips Catherine M CM

The American journal of clinical nutrition 20190601 6

<h4>Background</h4>Maternal caffeine intake is associated with adverse birth outcomes, but its long-term influence on offspring adiposity outcomes is not well studied. Furthermore, few studies have investigated paternal and grandparental caffeine intake in relation to offspring outcomes.<h4>Objective</h4>To study the associations between maternal, paternal, and grandparental caffeine intake and offspring childhood adiposity.<h4>Design</h4>The core study sample consists of 558 mother-child pairs ...[more]

PMID: 31136661

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Project description:BackgroundMaternal polyunsaturated fatty acid (PUFA) concentrations during pregnancy may have persistent effects on growth and adiposity in the offspring. A suboptimal maternal diet during pregnancy might lead to fetal cardiometabolic adaptations with persistent consequences in the offspring.ObjectiveWe examined the associations of maternal PUFA concentrations during pregnancy with childhood general and abdominal fat-distribution measures.DesignIn a population-based, prospective cohort study of 4830 mothers and their children, we measured maternal second-trimester plasma n-3 (ω-3) and n-6 (ω-6) PUFA concentrations. At the median age of 6.0 y (95% range: 5.6, 7.9 y), we measured childhood body mass index (BMI), the fat mass percentage, and the android:gynoid fat ratio with the use of dual-energy X-ray absorptiometry and measured the preperitoneal abdominal fat area with the use of ultrasound. Analyses were adjusted for maternal and childhood sociodemographic- and lifestyle-related characteristics.ResultsWe observed that higher maternal total n-3 PUFA concentrations, and specifically those of eicosapentaenoic acid, docosapentaenoic acid, and docosahexaenoic acid, were associated with a lower childhood total-body fat percentage and a lower android:gynoid fat mass ratio (P< 0.05) but not with childhood BMI and the abdominal preperitoneal fat mass area. Higher maternal total n-6 PUFA concentrations, and specifically those of dihomo-γ-linolenic acid, were associated with a higher childhood total-body fat percentage, android:gynoid fat mass ratio, and abdominal preperitoneal fat mass area (P< 0.05) but not with childhood BMI. In line with these findings, a higher maternal n-6:n-3 PUFA ratio was associated with higher childhood total-body and abdominal fat mass.ConclusionsLower maternal n-3 PUFA concentrations and higher n-6 PUFA concentrations during pregnancy are associated with higher body fat and abdominal fat in childhood. Additional studies are needed to replicate these observations and to explore the causality, the underlying pathways, and the long-term cardiometabolic consequences.

Project description:OBJECTIVES:To study the association between maternal caffeine intake during pregnancy and the child's weight gain and overweight risk up to 8 years. DESIGN:Prospective nationwide pregnancy cohort. SETTING:The Norwegian Mother and Child Cohort Study. PARTICIPANTS:A total of 50?943 mothers recruited from 2002 to 2008 and their children, after singleton pregnancies, with information about average caffeine intake assessed at mid-pregnancy. OUTCOME MEASURE:Child's body size information at 11 age points from 6 weeks to 8 years. We defined excess growth in infancy as a WHO weight gain z-score of >0.67 from birth to age 1?year, and overweight according to the International Obesity Task Force. We used a growth model to assess individual growth trajectories. RESULTS:Compared with pregnant women with low caffeine intake (<50?mg/day, 46%), women with average (50-199?mg/day, 44%), high (?200-299?mg/day, 7%) and very high (?300?mg/day, 3%) caffeine intakes had an increased risk of their child experiencing excess growth in infancy, after adjustment for confounders (OR=1.15, 95% CI 1.09 to 1.22, OR=1.30, 95%?CI 1.16 to 1.45, OR=1.66, 95%?CI 1.42 to 1.93, respectively). In utero exposure to any caffeine was associated with higher risk of overweight at age 3 years and 5 years, while the association persisted at 8 years, only for very high exposures. Any caffeine intake was associated with increased body mass index from infancy to childhood. Children prenatally exposed to caffeine intake >200?mg/day had consistently higher weight. Very high caffeine exposures were associated with higher weight gain velocity from infancy to age 8 years. CONCLUSION:Any caffeine consumption during pregnancy is associated with a higher risk of excess infant growth and of childhood overweight, mainly at preschool ages. Maternal caffeine intake may modify the overall weight growth trajectory of the child from birth to 8 years. This study adds supporting evidence for the current advice to reduce caffeine intake during pregnancy.

Project description:BackgroundEpigenetic mechanisms may underlie associations between maternal caffeine consumption and adverse childhood metabolic outcomes. However, limited studies have examined neonate DNA methylation (DNAm) patterns in the context of preconception or prenatal exposure to caffeine metabolites.ObjectivesWe examined preconception and pregnancy caffeine exposure with DNAm alterations in neonate cord blood (n = 378).MethodsIn a secondary analysis of the Effects of Aspirin in Gestation and Reproduction Trial (EAGeR), we measured maternal caffeine, paraxanthine, and theobromine concentrations from stored serum collected preconception (on average 2 months before pregnancy) and at 8 weeks of gestation. In parallel, self-reported caffeinated beverage intake was captured via administration of questionnaires and daily diaries. We profiled DNAm from the cord blood buffy coat of singletons using the MethylationEPIC BeadChip. We assessed associations of maternal caffeine exposure and methylation β values using multivariable robust linear regression. A false discovery rate (FDR) correction was applied using the Benjamini-Hochberg method.ResultsIn preconception, the majority of women reported consuming 1 or fewer servings/day of caffeine on average, and caffeine and paraxanthine metabolite levels were 88 and 36 µmol/L, respectively. Preconception serum caffeine metabolites were not associated with individual cytosine-guanine (CpG) sites (FDR >5%), though pregnancy theobromine was associated with DNAm at cg09460369 near RAB2A (β = 0.028; SE = 0.005; FDR P = 0.012). Preconception self-reported caffeinated beverage intake compared to no intake was associated with DNAm at cg09002832 near GLIS3 (β = -0.013; SE = 0.002; FDR P = 0.036). No associations with self-reported intake during pregnancy were found.ConclusionsFew effects of maternal caffeine exposure on neonate methylation differences in leukocytes were identified in this population with relatively low caffeine consumption.

Project description:Excessive early childhood adiposity is a prevalent and increasing concern in many parts of the world. Parental obesity is one of the several factors previously associated with infant and early childhood weight, length and adiposity. Parental obesity represents a surrogate marker of the complex interplay among genetic, epigenetic and shared environmental factors, and is potentially modifiable. The relative contributions of maternal and paternal body mass index (BMI) to infant and early childhood growth, as well as the timing of such effects, have not been firmly established.Utilizing serial infant measurements and growth curve modelling, this is the largest study to fully characterize and formally compare associations between maternal and paternal BMI and offspring growth across the entire infancy and early childhood period. Maternal obesity is a stronger determinant of offspring BMI than paternal obesity at birth and from 2 to 3 years of age, suggesting that prevention efforts focused particularly on maternal lifestyle and BMI may be important in reducing excess infant BMI. The observation that maternal BMI effects are not constant, but rather present at birth, wane and re-emerge during late infancy, suggests that there is a window of opportunity in early infancy when targeted interventions on children of obese mothers may be most effective.Parental obesity influences infant body size. To fully characterize their relative effects on infant adiposity, associations between maternal and paternal body mass index (BMI) category (normal: ?25?kg?m(-2) , overweight: 25?- <30?kg?m(-2) , obese: ?30?kg?m(-2) ) and infant BMI were compared in Fels Longitudinal Study participants.A median of 9 serial weight and length measures from birth to 3.5 years were obtained from 912 European American children born in 1928-2008. Using multivariable mixed effects regression, contributions of maternal vs. paternal BMI status to infant BMI growth curves were evaluated. Cubic spline models also included parental covariates, infant sex, age and birth variables, and interactions with child's age.Infant BMI curves were significantly different across the three maternal BMI categories (Poverall ?<?0.0001), and offspring of obese mothers had greater mean BMI at birth and between 1.5 and 3.5 years than those of over- and normal weight mothers (P???0.02). Average differences between offspring of obese and normal weight mothers were similar at birth (0.8?kg?m(-2) , P?=?0.0009) and between 2 and 3.5 years (0.7-0.8?kg?m(-2) , P?<?0.0001). Infants of obese fathers also had BMI growth curves distinct from those of normal weight fathers (P?=?0.02). Infant BMI was more strongly associated with maternal than paternal obesity overall (P?<?0.0001); significant differences were observed at birth (1.11?kg?m(-2) , P?=?0.006) and from 2 to 3 years (0.62?kg?m(-2) , P3 years ?=?0.02).At birth and in later infancy, maternal BMI has a stronger influence on BMI growth than paternal BMI, suggesting weight control in reproductive age women may be of particular benefit for preventing excess infant BMI.

Dataset Information

Maternal, but not paternal or grandparental, caffeine intake is associated with childhood obesity and adiposity: The Lifeways Cross-Generation Cohort Study.

Publications

Maternal, but not paternal or grandparental, caffeine intake is associated with childhood obesity and adiposity: The Lifeways Cross-Generation Cohort Study.

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