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The benefits of breastfeeding for the health and wellbeing of both infants and mothers are well documented, yet global breastfeeding rates are low. One factor associated with low breast feeding is maternal body mass index (BMI), which is used as a measure of obesity. The negative relationship between maternal obesity and breastfeeding is likely caused by a variety of social, psychological, and physiological factors. Maternal obesity may also have a direct biological association with breastfeeding through changes in maternal DNA methylation. Here, we investigate this potential biological association using data from a UK-based cohort study, the Avon Longitudinal Study of Parents and Children (ALSPAC). We find that pre-pregnancy body mass index (BMI) is associated with lower initiation to breastfeed and shorter breastfeeding duration. We conduct epigenome-wide association studies (EWAS) of pre-pregnancy BMI and breastfeeding outcomes, and run candidate-gene analysis of methylation sites associated with BMI identified via previous meta-EWAS. We find that DNA methylation at cg11453712, annotated to PHTP1, is associated with pre-pregnancy BMI. From our results, neither this association nor those at candidate-gene sites are likely to mediate the link between pre-pregnancy BMI and breastfeeding.

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BACKGROUND: The importance of the maternal-infant dyad in the genesis of nonalcoholic fatty liver disease (NAFLD) is of increasing interest. The Avon Longitudinal Study of Parents and Children (ALSPAC) showed that at age 24, 1 in 5 had NAFLD measured by transient elastography and controlled attenuation parameter (CAP). Our aim was to investigate the association between breastfeeding duration and maternal pre-pregnancy BMI on offspring NAFLD in young adulthood. METHODS: 4021 participants attended clinic for FibroScan and CAP measurement using Echosens 502 Touch®. 440 participants with Alcohol Use Disorders were excluded. Offspring of 100 non-singleton pregnancies were excluded. 2961 valid CAP measurements for NAFLD were analysed. Exposures of interest were breastfeeding of any duration, ≥6months exclusive breastfeeding, and maternal pre-pregnancy BMI. Multivariable regression models estimated the odds of NAFLD at 24 years. We performed a paternal negative control test to explore residual confounding in the analyses of pre-pregnancy BMI. FINDINGS: There was a modest inverse association of exclusive and non-exclusive breastfeeding ≥6 months having a protective effect on NAFLD in offspring (OR 0·92 [95%CI 0·66-1·27] and OR 0·90 [0·67-1·21] respectively).The odds of offspring NAFLD in overweight pre-pregnancy maternal BMI and paternal BMI was OR 2·09 [1·62-2·68] and OR 1·33 [95%CI 1·07-1·65] respectively, with the ratio of effect sizes OR 1·57 [1·11-2·22]. Similarly, odds of offspring NAFLD with obese pre-pregnancy maternal BMI and paternal BMI was OR 2·66 [1·71-4·14] and OR 1·35 [0·91-2·00] respectively, with the ratio of effect sizes OR 1·98 [1·05-3·74]. INTERPRETATION: Higher maternal pre-pregnancy BMI was associated with offspring NAFLD, having accounted for shared parental confounding. We did not replicate previous work that found a strong association between breastfeeding and NAFLD. FUNDING: Medical Research Council UK, Alcohol Research UK, David Telling Charitable Trust.

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Few studies have examined the possibility that pre- and post-natal factors may be non-linearly associated with later physical activity. We used data from the Norwegian Mother, Father and Child Cohort study (MoBa) and the Medical Birth Registry of Norway (MBRN), including 48 672 children with available data on leisure time physical activity (LTPA) at child's age 7 years. Restricted cubic and linear splines or linear regression was used to examine the associations between maternal pre-pregnancy BMI, birth weight for gestational age, and infant weight gain from birth to 1 year with LTPA (frequency/wk) in 7-year-old children. The results suggest no associations between maternal pre-pregnancy BMI, birth weight, and infant weight gain on subsequent LTPA in girls. Maternal pre-pregnancy BMI and birth weight may be non-linearly associated with LTPA in 7-year-old boys. Infant weight gain (change in weight z-score from birth to 1 year) may be weakly linearly associated with LTPA in boys. Pre- and post-natal factors may therefore influence LTPA in childhood differently in boys and girls. Maternal pre-pregnancy BMI and birth weight are positively associated with LTPA at the lower ends of the maternal pre-pregnancy BMI and birth weight continuums in boys. The negative associations at the higher ends of the continuums and the positive association between infant weight gain and LTPA in boys may not be important and needs further replication.

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OBJECTIVES: High maternal pre-pregnancy body mass index (BMI), high birth weight, and rapid infant weight gain are associated with increased risk of childhood obesity. We examined whether moderate-to-vigorous physical activity (MVPA) or vigorous physical activity (VPA) in 9- to 12-year-olds modified the associations between these early life risk factors and subsequent body composition and BMI. METHODS: We used data from a sub-cohort of the Norwegian Mother and Child Cohort Study (MoBa), including 445 children with available data on accelerometer assessed physical activity (PA). All participants had data on BMI, 186 of them provided data on body composition (dual energy X-ray absorptiometry (DXA)). We used multiple regression analyses to examine the modifying effect of PA by including interaction terms. RESULTS: Maternal pre-pregnancy BMI and infant weight gain were more strongly related to childhood body composition in boys than in girls. Higher VPA attenuated the association between maternal pre-pregnancy BMI and BMI in boys (low VPA: B = 0.32, 95% CI = 0.22, 0.41; high VPA B = 0.22, 95% CI = 0.12, 0.31). Birth weight was unrelated to childhood body composition, and there was no effect modification by PA. PA attenuated the associations between infant weight gain and childhood fat mass (low MVPA: B = 2.32, 95% CI = 0.48, 4.17; high MVPA: B = 1.00, 95% CI = 0.10, 1.90) and percent fat (low MVPA: B = 3.35, 95% CI = 0.56, 6.14; high MVPA: B = 1.41, 95% CI = -0.06, 2.87) in boys, but not girls. CONCLUSION: Findings from this study suggest that MVPA and VPA may attenuate the increased risk of an unfavorable body composition and BMI due to high maternal pre-pregnancy BMI and rapid infant weight gain in boys, but not in girls.

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Maternal body mass index (BMI) before pregnancy is known to affect both fetal growth and later-life health of the newborn, yet the implicated molecular mechanisms remain largely unknown. As the master regulator of the fetal environment, the placenta is a valuable resource for the investigation of processes involved in the developmental programming of metabolic health. We conducted a genome-wide placental transcriptome study aiming at the identification of functional pathways representing the molecular link between maternal BMI and fetal growth. We used RNA microarray (Agilent 8 × 60 K), medical records, and questionnaire data from 183 mother-newborn pairs from the ENVIRONAGE birth cohort study (Flanders, Belgium). Using a weighted gene co-expression network analysis, we identified 17 correlated gene modules. Three of these modules were associated with both maternal pre-pregnancy BMI and newborn birth weight. A gene cluster enriched for genes involved in immune response and myeloid cell differentiation was positively associated with maternal BMI and negatively with low birth weight. Two other gene modules, upregulated in association with maternal BMI as well as birth weight, were involved in processes related to organ and tissue development, with blood vessel morphogenesis and extracellular matrix structure as top Gene Ontology terms. In line with this, erythrocyte-, angiogenesis-, and extracellular matrix-related genes were among the identified hub genes. The association between maternal BMI and newborn weight was significantly mediated by gene expression for 5 of the hub genes (FZD4, COL15A1, GPR124, COL6A1, and COL1A1). As some of the identified hub genes have been linked to obesity in adults, our observation in placental tissue suggests that biological processes may be affected from prenatal life onwards, thereby identifying new molecular processes linking maternal BMI and fetal metabolic programming.

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OBJECTIVE: The aim of the present study is to identify the average effect across different time points and to specify the time effects of maternal pre-pregnancy BMI and weekly gestational weight gain on the mental development and physical growth of infants. METHODS: The present cohort study used a repeated measures study design that began in 2004 with follow up at 3, 6, 12, 18, and 24 months of age. The participants were a subset from a controlled, cluster-randomized, double-blind trial. Bayley Scales of Infant Development (BSID) were used to estimate the mental development of infants. A generalized estimating equation linear model was used to estimate the effects of maternal BMI and weight gain. RESULTS: The average effect of maternal BMI and weight gain on the weight for age Z scores (WAZ), length for age Z scores (LAZ) and mental development index (MDI) across the different time points of infants was significant. In addition, the maternal BMI and weight gain were positively and significantly associated with the WAZ and LAZ in infants of different ages. However, the effect of weekly gestational weight gain was significant only during the earlier period of life (3 months, Coefficient: 11.15, 95%CI: 4.89-17.41). CONCLUSIONS: Our results indicate positive effects of pre-pregnancy and prenatal nutrition on the physical growth of infants. Weekly gestational weight gain of the pregnant women had a positive effect on the mental development of the infants, but this effect appears to decline over time.

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AIMS/HYPOTHESIS: Accumulating evidence suggests an impact of gestational weight gain (GWG) on pregnancy outcomes; however, data on cardiometabolic risk factors later in life have not been comprehensively studied. This study aimed to evaluate the relationship between GWG and cardiometabolic risk in offspring aged 7 years. METHODS: We included a total of 905 mother-child pairs who enrolled in the follow-up visit of the multicentre Hyperglycemia and Adverse Pregnancy Outcome study, at the Hong Kong Centre. Women were classified as having gained weight below, within or exceeding the 2009 Institute of Medicine (IOM) guidelines. A standardised GWG according to pre-pregnancy BMI categories was calculated to explore for any quadratic relationship. RESULTS: Independent of pre-pregnancy BMI, gestational hyperglycaemia and other confounders, women who gained more weight than the IOM recommendations had offspring with a larger body size and increased odds of adiposity, hypertension and insulin resistance (range of p values of all the traits: 4.6 × 10-9 < p < 0.0390) than women who were within the recommended range of weight gain during pregnancy. Meanwhile, women who gained less weight than outlined in the recommendations had offspring with increased risks of hypertension and insulin resistance, compared with those who gained weight within the recommended range (7.9 × 10-3 < p < 0.0477). Quadratic relationships for diastolic blood pressure, AUC for insulin, pancreatic beta cell function and insulin sensitivity index were confirmed in the analysis of standardised GWG (1.4 × 10-3 < pquadratic < 0.0282). Further adjustment for current BMI noticeably attenuated the observed associations. CONCLUSIONS/INTERPRETATION: Both excessive and inadequate GWG have independent and significant impacts on childhood adiposity, hypertension and insulin resistance. Our findings support the notion that adverse intrauterine exposures are associated with persistent cardiometabolic risk in the offspring.

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OBJECTIVE: To assess the association between maternal prepregnancy body mass index and adequacy of pregnancy weight gain in relation to neurocognitive function in school-aged children born extremely preterm. STUDY DESIGN: Study participants were 535 ten-year-old children enrolled previously in the prospective multicenter Extremely Low Gestational Age Newborns cohort study who were products of singleton pregnancies. Soon after delivery, mothers provided information about prepregnancy weight. Prepregnancy body mass index and adequacy of weight gain were characterized based on this information. Children underwent a neurocognitive evaluation at 10 years of age. RESULTS: Maternal prepregnancy obesity was associated with increased odds of a lower score for Differential Ability Scales-II Verbal IQ, for Developmental Neuropsychological Assessment-II measures of processing speed and visual fine motor control, and for Wechsler Individual Achievement Test-III Spelling. Children born to mothers who gained an excessive amount of weight were at increased odds of a low score on the Oral and Written Language Scales Oral Expression assessment. Conversely, children whose mother did not gain an adequate amount of weight were at increased odds of a lower score on the Oral and Written Language Scales Oral Expression and Wechsler Individual Achievement Test-III Word Reading assessments. CONCLUSION: In this cohort of infants born extremely preterm, maternal obesity was associated with poorer performance on some assessments of neurocognitive function. Our findings are consistent with the observational and experimental literature and suggest that opportunities may exist to mitigate risk through education and behavioral intervention before pregnancy.

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PURPOSE: Body size, from birth throughout adulthood, is associated with breast cancer risk, but few studies have investigated early-life body size and benign breast disease (BBD), a well-established breast cancer risk factor. We consider whether prenatal factors and size at birth, 10, 18 year, and intervening growth, are related to BBD risk. METHODS: The Growing Up Today Study includes 9032 females who completed questionnaires annually from 1996 to 2001, then 2003, 2005, 2007, 2010, and 2013. In 1996, their mothers provided pregnancy-related data. From 2005 to 2013, participants (18 year+) reported whether they had ever been diagnosed with biopsy-confirmed BBD (N = 142 cases). RESULTS: Girls had greater adiposity (BMI; kg/m2) at 10 year if they were larger at birth, if mother's pre-pregnancy BMI was higher, or if gestational weight gain was greater (all p < .01). Maternal height was (positively) associated (p < .05) with adolescent peak height growth velocity (PHV; in./year). Greater 10 year adiposity was associated with lower PHV and less height growth 10-18 year (both p < .01). Adiposity at 10 year was inversely associated with BBD (OR 0.83/(kg/m2), p < .01) as was increasing adiposity 10-18 year (OR 0.85/(kg/m2), p = .01). In a separate model, 10 year height (OR 1.13/in., p = .02) and height growth 10-18 year (OR 1.19/in.; p < .01) were positively associated. PHV was similarly positively associated (OR 2.58, p = .01, fastest versus slowest growth quartiles). In a multivariable model of BBD risk, gestational weight gain (daughters at highest risk if <20 lb gained), PHV (slowest growing girls at lowest risk), age 10 year height (positive), and BMI (inverse) were the most critical childhood risk factors (each p < .05). CONCLUSIONS: Body size factors from pregnancy through adolescence were independently associated with BBD risk in young women.

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Benign breast disease (BBD) is a well-established risk factor for breast cancer, but little work has considered a girl's early life and her risk for BBD in adulthood. We investigated factors, from pre-conception through infant feeding practices, in relation to subsequent BBD risk in young women. The Growing Up Today Study (GUTS) includes 9032 females, born 1980-1987, who completed questionnaires annually from 1996 through 2001, then 2003, 2005, 2007, 2010, and 2013. In 1996, their mothers provided each participant's birth weight and length, gestational age, biological father's height, and infant feeding factors (e.g., breast-fed, type of formula). In 1999, their mothers reported maternal pre-pregnancy weight and weight gain during index pregnancy. Beginning in 2005, daughters (18 years+) reported whether they had ever been diagnosed with biopsy-confirmed BBD (n = 142 cases, through 2013). Logistic regression estimated associations between early life factors and biopsy-confirmed BBD. Girls whose mother's BMI prior to pregnancy was 20-25 kg/m(2) were at lower risk of BBD as young women (OR = 0.66, p = 0.04, vs. maternal pre-pregnancy BMI < 20). Girls whose mothers gained 20 + pounds (vs. <20 pounds) during pregnancy were at lower risk (among full-term singleton births: OR = 0.48, p = 0.007, if mother gained 20-35 pounds). However, neither birth weight nor BMI at birth were associated with subsequent BBD risk. We found no evidence that infant feeding practices were linked to BBD. A healthy maternal BMI before pregnancy and sufficient weight gain during pregnancy may produce daughters at lower risk for BBD as young women. Further examination of these findings is needed.

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