Maternal Prenatal Diet Research Articles

Maternal dietary patterns and placental outcomes among pregnant women in Los Angeles

IntroductionEpidemiological studies have linked prenatal maternal diet to fetal growth, but whether diet affects placental outcomes is poorly understood. MethodsWe collected past month dietary intake from 148 women in mid-pregnancy enrolled at University of California Los Angeles (UCLA) antenatal clinics from 2016 to 2019. We employed the food frequency Diet History Questionnaire II and generated the Healthy Eating Index-2015 (HEI-2015), the Alternate Healthy Eating Index for Pregnancy (AHEI-P), and the Alternate Mediterranean Diet (aMED). We conducted T2-weighted magnetic resonance imaging (MRI) in mid-pregnancy (1st during 14–17 and 2nd during 19–24 gestational weeks) to evaluate placental volume (cm3) and we measured placenta weight (g) at delivery. We estimated change and 95 % confidence interval (CI) in placental volume and associations of placenta weight with all dietary index scores and diet items using linear regression models. ResultsPlacental volume in mid-pregnancy was associated with an 18.9 cm3 (95 % CI 5.1, 32.8) increase per 100 gestational days in women with a higher HEI-2015 (≥median), with stronger results for placentas of male fetuses. We estimated positive associations between placental volume at the 1st and 2nd MRI and higher intake of vegetables, high-fat fish, dairy, and dietary intake of B vitamins. A higher aMED (≥median) score was associated with a 40.5 g (95 % CI 8.5, 72.5) increase in placenta weight at delivery, which was mainly related to protein intake. DiscussionPlacental growth represented by volume in mid-pregnancy and weight at birth is influenced by the quality and content of the maternal diet.

PSVIII-29 Nutritional Epigenetic Modifications in Beef Cattle

Abstract Nutrition of the beef cow during pregnancy influences fetal development and potential changes in phenotype. On average 9 to 10% of the beef cattle herd are below the optimal body condition score of 2.5/5 at both pre-breeding and pregnancy tests, indicating potential nutritional stress during gestation. Epigenetic modifications are reported to regulate the changes in phenotype due to maternal nutrition during gestation. Our objective was to evaluate the influence of maternal nutrition during gestation on possible epigenetic mechanisms regulating development and biological function in Longissimus dorsi (LD) and Semimembranosus (SM) muscles, and liver (LV) at slaughter in steer progeny born from dams fed two different planes of nutrition during gestation. We also wanted to explore if the genetic potential of the offspring for residual feed intake (RFI) would interact with prenatal maternal diet to have differential effects on these epigenetic mechanisms. Purebred Angus steer calves (n = 23) were born from dams which were fed a diet formulated for an average daily gain (ADG) of either 0.5 or 0.7 kg/d from 30 to 150 days of gestation. Mating was designed so that calves were born from parents with differential genetic potential for high or low RFI. Calves were raised together as per normal industry standards and fed to be slaughtered as finished steers at approximately 512.1 ± 10.1 days of age. One approximately 10 g sample each of LV, LD, and SM muscles was aseptically collected within 30 to 45 min post-mortem and snap frozen in liquid nitrogen and subsequently stored at -80°C. Both DNA and RNA were isolated from the tissue samples and investigated for differences in methylation and gene expression, respectively. Fifteen potentially differently methylated regions (DMRs) in the DNA were measured using EpiTYPER MassARRAY technology, while expression of genes corresponding to the potential DMRs was measured by the nCounter Element Tagset by NanoString technologies. Average methylation across each DMR as well as gene expression within each tissue was profiled using principal component analyses (PCA). Distinct clustering was seen within both DNA methylation and gene expression PCAs such that the two muscles were clustered together and were separate from DNA methylation and gene expression measured in LV, representing expected functional variation due to tissue type. Between LD and SM, methylation patterns in the two muscles overlap, while there is much less overlap in gene expression patterns. This implies that the methylation pattern between the two muscle types is relatively similar compared with their patterns in gene expression, and that smaller differences in DNA methylation may lead to relatively larger differences in gene expression. These analyses are an important first step to interrogate the quality of our data that will be further analyzed for responses to maternal diet treatment and selection for genetic potential for RFI.

Application of Life's Essential 8 to assess cardiovascular health during early childhood.

Assess cardiovascular health (CVH) during early childhood using the American Heart Association's recently updated construct, Life's Essential 8 (LE8); examine concordance in CVH status per LE8 versusLife's Simple 7 (LS7); and identify perinatal correlates of high CVH per LE8. We applied LE8 and LS7 to data from 305 children aged 4-7 years in Denver, CO; estimated % low, moderate, high, and optimal CVH; assessed concordance in CVH status based on LE8 and LS7 using contingency tables; and used multivariable logistic regression to identify early-life correlates of high CVH per LE8. Average age of children was 4.7±0.6 years,44.6% were female. No participants had low or optimal CVH,43.9% had high, and 56.1% had moderate CVH per LE8, whereas 33.4% had high and 66.6% had moderate CVH per LS7. Twenty-two percent had high CVH based on both constructs. Correlates of high CVH were maternal prenatal diet quality (odds ratioHealthy Eating Index score>vs. ≤57 =1.90 [1.12, 3.21]) and child age (odds ratioper 1 year =1.58 [1.04. 2.42]). LE8 yielded higher prevalence of high CVH than LS7 during early childhood, though there is modest concordance between the two constructs. Maternal diet is a potential modifiable target to optimize early-life CVH.

Nurturing the Early Life Gut Microbiome and Immune Maturation for Long Term Health.

Early life is characterized by developmental milestones such as holding up the head, turning over, sitting up and walking that are typically achieved sequentially in specific time windows. Similarly, the early gut microbiome maturation can be characterized by specific temporal microorganism acquisition, colonization and selection with differential functional features over time. This orchestrated microbial sequence occurs from birth during the first years of age before the microbiome reaches an adult-like composition and function between 3 and 5 years of age. Increasingly, these different steps of microbiome development are recognized as crucial windows of opportunity for long term health, primarily linked to appropriate immune and metabolic development. For instance, microbiome disruptors such as preterm and Cesarean-section birth, malnutrition and antibiotic use are associated with increased risk to negatively affect long-term immune and metabolic health. Different age discriminant microbiome taxa and functionalities are used to describe age-appropriate microbiome development, and advanced modelling techniques enable an understanding and visualization of an optimal microbiome maturation trajectory. Specific microbiome features can be related to later health conditions, however, whether such features have a causal relationship is the topic of intense research. Early life nutrition is an important microbiome modulator, and ‘Mother Nature’ provides the model with breast milk as the sole source of nutrition for the early postnatal period, while dietary choices during the prenatal and weaning period are to a large extent guided by tradition and culture. Increasing evidence suggests prenatal maternal diet and infant and child nutrition impact the infant microbiome trajectory and immune competence development. The lack of a universal feeding reference for such phases represents a knowledge gap, but also a great opportunity to provide adequate nutritional guidance to maintain an age-appropriate microbiome for long term health. Here, we provide a narrative review and perspective on our current understanding of age-appropriate microbiome maturation, its relation to long term health and how nutrition shapes and influences this relationship.

Maternal Dietary Quality and Dietary Inflammation Associations with Offspring Growth, Placental Development, and DNA Methylation

The ‘Developmental Origins of Health and Diseases’ hypothesis posits that prenatal maternal diet influences offspring growth and later life health outcomes. Dietary assessment has focused on selected nutrients. However, this approach does not consider the complex interactions between foods and nutrients. To provide a more comprehensive approach to public health, dietary indices have been developed to assess dietary quality, dietary inflammation and risk factors for non-communicable diseases. Thus far, their use in the context of placental development is limited and associations with offspring outcomes have been inconsistent. Although epidemiological studies have focused on the role of maternal diet on foetal programming, the underlying mechanisms are still poorly understood. Some evidence suggests these associations may be driven by placental and epigenetic changes. In this narrative review, we examine the current literature regarding relationships between key validated diet quality scores (Dietary Inflammatory Index [DII], Mediterranean diet [MD], Healthy Eating Index [HEI], Alternative Healthy Eating Index [AHEI], Dietary Approaches to Stop Hypertension [DASH], Glycaemic Index [GI] and Glycaemic Load [GL]) in pregnancy and birth and long-term offspring outcomes. We summarise findings, discuss potential underlying placental and epigenetic mechanisms, in particular DNA methylation, and highlight the need for further research and public health strategies that incorporate diet quality and epigenetics.

Ambient air pollution, psychological stress, and early childhood respiratory outcomes: Modifying effects of prenatal maternal diet, sex, and race/ethnicity

BACKGROUND AND AIM: Many lower income, racially/ethnically mixed communities experience co-occurring environmental hazards (i.e., pollutants, social inequities and related stress, poorer access to healthy foods) contributing to respiratory disease. Starting {in utero}, fine particulate matter (PM₂.₅) and stress disrupt similar but not completely overlapping processes, including oxidative stress, influencing respiratory health. Antioxidant intake can have protective effects. We examined associations among prenatal PM₂.₅, maternal stress, and antioxidant intake in relation to early childhood wheeze in a longitudinal pregnancy cohort in the Northeastern United States (N=539). METHODS: Daily prenatal PM₂.₅ exposure was estimated using a satellite-based spatiotemporally resolved model. Women completed the Lifetime Stressor Checklist-Revised (LSC-R). A prenatal antioxidant index (AI) was based on average percentile intake of beta-carotene, vitamins (A,C,E), zinc, magnesium, and selenium. Mothers reported child wheeze with follow-up to 4.1±2.8 years. Logistic regression was used to examine effects of prenatal AI and LSC-R on repeated wheeze (≥2 episodes); effect modification was explored in stratified models. Bayesian distributed lag interaction models (BDLIMs) were used to examine associations between prenatal PM₂.₅ exposure on wheeze, and effect modification by AI, race/ethnicity, and child sex. Covariates included maternal age, education, asthma, and temperature. RESULTS:Women were 39.3% black and 33% Hispanic with 35.6% reporting ≤high school education; 20.3% of children had repeated wheeze. The association between higher AI and decreased wheeze was significant only in blacks (Odds Ratio, OR=0.37, 95% confidence interval, CI: 0.19-0.73 per interquartile range increase). Higher stress was associated with repeated wheeze when AI was below the median, especially among blacks/Hispanics [OR=1.04 (1.01-1.06)]. BDLIMs found that cumulative effect on repeated wheeze per μg/m³ increase in PM₂.₅ across pregnancy was only significant in boys born to black mothers with low antioxidant intake [OR=1.2 (1.01-1.59)]. CONCLUSIONS:Relationships among prenatal PM₂.₅, stress, antioxidant intake, and child wheeze are complex and are modified by race/ethnicity and child sex. KEYWORDS: particulate matter, prenatal stress, nutrition, antioxidants, pediatric respiratory outcomes

Impact of genetic potential for residual feed intake and diet fed during early- to mid-gestation in beef heifers on carcass characteristics and meat quality attributes of their castrated male offspring

Carcass attributes of steers were examined for influences of selection for residual feed intake (RFI), and exposure to different levels of prenatal nutrition. Heifers characterized for RFI corrected for backfat were mated to bulls with genetic potential for either High-RFI or Low-RFI, such that the progeny were expected to be H/H or L/L RFI (sire/dam). Pregnant heifers were assigned to a low diet (Ldiet; 0.40 kg/d ADG), or moderate diet (Mdiet; 0.57 kg/d ADG), from 30 to 150 days of gestation, after which all heifers were managed similarly. Steer offspring (n = 23) were also managed similarly until slaughter. Dressing percentage of steers from H-RFI dams/sires exposed to Ldiet during gestation was lower than all other groups (P = 0.02). Marbling was greater for steers from H-RFI parents, as was fat content of longissimus thoracis et lumborum and triceps brachii (P ≤ 0.02). Results suggest that parental selection for RFI and prenatal maternal diet can influence carcass characteristics of progeny.

A Prospective Study of Prenatal Maternal Dietary Patterns and Offspring Adipokine Levels During Adolescence

ObjectivesMaternal diet during pregnancy has been associated with offspring adipokine levels related to insulin resistance and hyperlipidemia during infancy. However, whether this relationship persists into adolescence is unknown. We examined the association between maternal prenatal diet patterns with adolescent leptin and adiponectin levels a Mexico City cohort. MethodsData from 379 mother-adolescent dyads from the Mexico City ELEMENT cohort were analyzed. Diet patterns were derived from principal component analysis of food frequency questionnaire data collected during pregnancy trimesters. Adolescent serum leptin and adiponectin were measured at ages 10–17. Information on maternal covariates was measured during pregnancy. Multiple linear regression was used to examine overall and sex-stratified associations between quartiles of diet patterns with leptin and adiponectin, adjusting for maternal marital status, education, and parity. ResultsThree maternal diet patterns were identified: Prudent Diet (PD), high in fish and vegetables, the High Meat & Fat Diet (HMFD), high in pork and processed meats, and the Transitioning Diet (TD), high in corn tortillas and sugar beverages. At follow-up, the mean (SD) of leptin and adiponectin were 24.3 (18.2) ng/ml and 11.7 (3.9) ng/ml. A significant positive association was demonstrated between first trimester TD scores and adipokines in girls. In a multivariate-adjusted model, compared to girls in the lowest quartile (Q1) of the TD pattern, the highest quartile of the TD pattern (Q4) had 10.39 ng/mL higher leptin (95% CI: 3.1, 17.6; p for trend = 0.0024). In addition, compared to girls in the lowest quartile (Q1) of the TD pattern, those in the third quartile (Q3) of the TD pattern had 1.86 ng/mL lower adiponectin (95% CI: –3.5, –0.2; p for trend = 0.168). Associations were mostly consistent across all trimesters. ConclusionsDuring pregnancy, a Transitioning Diet pattern was positively associated with leptin and non-monotonically inversely associated with adiponectin in females. Findings suggest maternal diet patterns during pregnancy may influence offspring leptin and adiponectin levels in adolescent girls. Funding SourcesFunded by grant P01ES022844.

Impact of prenatal maternal nutrition and parental residual feed intake (RFI) on mRNA abundance of metabolic drivers of growth and development in young Angus bulls

• Muscular, hepatic, and testicular MEF2A expression associated with feed efficiency • Longissimus MEF2A expression was also affected by prenatal maternal nutrition • Hepatic PCDH19 expression was increased in bulls exposed to low prenatal nutrition • Muscular/hepatic/testicular gene expression correlated with measures of intake • Muscular/hepatic/testicular gene expression correlated with final/trimmed weight Approximately 70% of the cost of beef production is impacted by feed utilization. Maximizing production efficiency of beef cattle requires not only genetic selection to maximize feeding efficiency (i.e. residual feed intake - RFI), but also adequate nutrition throughout all stages of growth and development to maximize productivity of growth and reproductive capacity, even during gestation. Nutrient restriction during gestation has been shown to negatively affect post-natal growth and development. This, when combined with efforts to minimize RFI, may significantly affect energy partitioning in the offspring and subsequently important performance traits. Therefore, we decided to investigate the impacts of prenatal under-nutrition during the first half of gestation, as well as selection for divergent RFI, upon gene expression in select tissues, including Longissimus thoracis (LT) and semimembranosus (SM) muscles, liver, and testis, in Angus bull progeny. The genes monitored in this study included metabolic drivers of animal growth, especially muscle growth and development, and those that were aspects of detoxification/immune function. The results showed that the mRNA abundance of protocadherin 19 [ PCDH19 ] in liver, and myocyte enhancer factor 2A [ MEF2A ] in LT muscle, was significantly higher in Low-diet (Ldiet), and Normal-diet (Ndiet) prenatal maternal diet groups, respectively. The results also showed that in all four tissues, expression of MEF2A was significantly higher in the Low-RFI (LRFI) group as compared to its High-RFI (HRFI) counterpart. We also reported correlations between gene expression in these four tissues with phenotypic measures of feed efficiency and body weight.

Maternal Dietary Factors and the Risk of Autism Spectrum Disorders: A Systematic Review of Existing Evidence.

Prenatal maternal diet is a critical factor in offspring neurodevelopment. Emerging evidence suggests that prenatal diet may also play a role in the etiology autism spectrum disorder (ASD). This review summarizes studies published in English that examined prenatal nutrients or maternal diet in association with ASD from PubMed as of July 2020. Thiry-six studies from nine countries were included in this systematic review; these focused on multivitamin (n = 5), prenatal vitamin (n = 3), folic acid (FA; n = 14), Vitamin D (n = 11), polyunsaturated fatty acid or fish/supplement intake (n = 7), iron (n = 3), Vitamin B12 (n = 1), calcium (n = 1), magnesium (n = 1), and broad maternal dietary habits (n = 3). Overall, higher or moderate intake of prenatal/multivitamin, FA, and Vitamin D was associated with reductions in odds of ASD, though results have not been uniform and there is a need to clarify differences in findings based on biomarkers versus reported intake. Evidence was inconclusive or insufficient for other nutrients. Differences in the timing and measurement of these dietary factors, as well as potential residual confounding, may contribute to existing discrepancies. Key areas for future research to better understand the role of maternal diet in ASD include the need to address potential critical windows, examine the combined effect of multiple nutrients, and consider interactions with genetic or environmental factors. LAY SUMMARY: Maternal diet during pregnancy is important for child neurodevelopment. We reviewed 36 studies examining maternal diet and autism spectrum disorder (ASD) and found that prenatal vitamin/multivitamin use and adequate intake of folic acid and Vitamin D were each associated with lower likelihood of having a child with ASD. Future studies on these and other dietary factors are needed to better understand the role of maternal diet in the development of ASD. Autism Res 2020, 13: 1634-1658. © 2020 International Society for Autism Research and Wiley Periodicals LLC.

A Prospective Study of the Relationship of Infant Adiposity with Maternal Prenatal and Postnatal Diet Quality

Abstract Objectives This study examines relationships of maternal prenatal and postnatal diet quality with infant birth size and growth, which are known risk factors for child obesity. Methods Women completed six 24-hour diet recalls (1 per pregnancy trimester and at 6 weeks, 6 months, and 12 months postpartum); infant anthropometrics were obtained at birth (n = 331 mother-child dyads), 6 weeks, 6 months and 12 months of age. Prenatal and postnatal Healthy Eating Index 2015 total (HEI), adequacy (HEI-adq) and moderation (HEI-mod) scores were calculated by combining recalls across pregnancy and across postpartum. Linear mixed models estimated associations of infant weight-for-length z-scores (WFLz) with prenatal and postnatal diet quality. Logistic regressions estimated odds of small-for-gestational age (SGA, <10th percentile) and large-for-gestational age (LGA, >90th percentile) associated with maternal prenatal diet quality. Covariates included maternal height, demographics, delivery mode, child sex, and gestational age at delivery. Sensitivity analyses examined whether associations were robust to inclusion of maternal total energy intake or early pregnancy BMI. Results WFLz was inversely associated with prenatal HEI (β±SE = −0.02 ± 0.005, P = 0.004) and HEI-mod (β ± SE = −0.04 ± 0.01, P < 0.001), and with postnatal HEI (β ± SE = −0.01 ± 0.005, P = 0.01) and HEI-adq (β ± SE = −0.02 ± 0.007, P = 0.005). SGA and LGA occurred for 92 (7%) and 172 (12%) babies, respectively. LGA was inversely associated with prenatal HEI (OR = 0.94, 95% CI: 0.90–0.98), HEI-mod (OR = 0.83, 95% CI: 0.74–0.83) and HEI-adq (OR = 0.95, 95% CI: 0.90–1.01). SGA was not associated with prenatal diet quality. Associations were not changed when adjusted for energy intake but were modestly attenuated when adjusted for BMI. Conclusions Higher maternal prenatal and postnatal diet quality were associated with more favorable indicators of infant adiposity from birth through 12 months of age. Interventions are needed to determine whether targeting both prenatal and postnatal diet may lead to improved infant adiposity development. Funding Sources This research was supported by the NICHD Intramural Research Program.

Associations of maternal diet with infant adiposity at birth, 6 months and 12 months

ObjectivesTo assess associations between maternal prenatal diet quality and infant adiposity.DesignThe design was a prospective birth cohort.SettingWe used data from the Nurture study, a cohort of women and their infants...

The effect of dietary fat on behavior in mice.

Obesity is linked to cognitive dysfunction in humans and rodents, and its effects can be passed on to the next generation. However, the extent of these effects is not well understood. The purpose of this study was to determine the effect of a prenatal maternal high-fat diet and an individual high-fat diet in inbred mice. We varied maternal diet and offspring diet to test the hypothesis that a high-fat diet would increase anxiety, reduce activity levels, and impair nest-building. First, we fed a high-fat (HF) or low-fat (LF) diet to genetically identical female Small (SM/J) mice and mated them with LF males. We cross-fostered all offspring to LF-fed SM/J nurses and weaned them onto an HF or LF diet. We weighed the mice weekly and we tested anxiety with the Open Field Test, activity levels with instantaneous scan sampling, and nest building using the Deacon Scale. Diet significantly affected weight, with HF females weighing 28.2g (± 1.4g SE) and LF females weighing 15.1g (± 1.6g SE) at 17weeks old. The offspring's own diet had major behavioral effects. HF mice produced more fecal boli and urinations in the Open Field Test, built lower-quality nests, and had lower activity in adulthood than LF mice. The only trait that a prenatal maternal diet significantly affected was whether the offspring built their nests inside or outside of a hut. Offspring diet, but not prenatal maternal diet, affected a wide range of behaviors in these mice.

Prenatal Diet and the Development of Childhood Allergic Diseases: Food for Thought.

The development of allergic disease is shaped by genetics and the environment, including diet. Many studies suggest a role for maternal diet during pregnancy. In this article, we discuss potential mechanisms by which specific nutrients, particular foods, and dietary patterns may influence allergic disease development and review studies examining the relationship between prenatal diet and the risk of childhood allergy. The combination of in utero exposures and genetic predisposition may contribute to the development of allergic disease by altering immune and organ development. Inflammation predominates in the first and third trimesters whereas the second trimester is characterized by anti-inflammatory and Th2 immune responses. Maternal dietary exposures during pregnancy may interact with inherited genetic risk factors influence immune system development. There are varied results regarding the impact of maternal prenatal diet on the development of childhood allergies. Well-designed randomized controlled studies are needed to clarify this area.

Neurodevelopment in 3–4 year old children exposed to maternal hyperglycemia or adiposity in utero

BackgroundPrenatal exposure to maternal metabolic complications has been linked to offspring neurodevelopmental problems. However, no studies investigating these links have examined the role of maternal prenatal diet. AimsTo determine if prenatal exposure to maternal adiposity or hyperglycemia is associated with neurodevelopmental problems in 3–4 year old children, and if links persist following adjustment for confounding variables, including prenatal diet. Method808 mother-child pairs from the Maternal-Infant Research on Environmental Chemicals-Child Development Plus cohort were used to examine associations between pre-pregnancy body mass index (BMI), hyperglycemia and offspring verbal, performance and full-scale IQ scores, as well as internalizing and externalizing problems. Associations were examined before and after adjustment for prenatal diet along with home environment, maternal depression, education and prenatal smoking. Semi-partial correlations were examined post-hoc to assess the impact of each confounder in the adjusted models. ResultsIn the unadjusted models, BMI and hyperglycemia predicted lower verbal and full-scale IQ. BMI was also linked to externalizing problems. However, associations were not significant after adjustment. In adjusted models, post-hoc analysis revealed that prenatal diet and home environment accounted for significant variance in verbal and full-scale IQ. The home environment and maternal depression accounted for significant variance in externalizing problems. ConclusionIn the adjusted models, maternal metabolic complications were not associated with offspring neurodevelopment. Even while adjusting for well-known risk factors for adverse offspring cognition (home environment, maternal depression), we show for the first time that maternal prenatal diet is an important confounder of the links between maternal metabolic complications and offspring cognition.

Maternal diet during pregnancy is related with the infant stool microbiome in a delivery mode-dependent manner

BackgroundThe gut microbiome has an important role in infant health and immune development and may be affected by early-life exposures. Maternal diet may influence the infant gut microbiome through vertical transfer of maternal microbes to infants during vaginal delivery and breastfeeding. We aimed to examine the association of maternal diet during pregnancy with the infant gut microbiome 6 weeks post-delivery in mother-infant dyads enrolled in the New Hampshire Birth Cohort Study. Infant stool samples were collected from 145 infants, and maternal prenatal diet was assessed using a food frequency questionnaire. We used targeted sequencing of the 16S rRNA V4-V5 hypervariable region to characterize infant gut microbiota. To account for differences in baseline and trajectories of infant gut microbial profiles, we stratified analyses by delivery mode.ResultsWe identified three infant gut microbiome clusters, characterized by increased abundance of Bifidobacterium, Streptococcus and Clostridium, and Bacteroides, respectively, overall and in the vaginally delivered infant stratum. In the analyses stratified to infants born vaginally and adjusted for other potential confounders, maternal fruit intake was associated with infant gut microbial community structure (PERMANOVA, p < 0.05). In multinomial logistic regression analyses, increased fruit intake was associated with an increased odds of belonging to the high Streptococcus/Clostridium group among infants born vaginally (OR (95% CI) = 2.73 (1.36, 5.46)). In infants delivered by Cesarean section, we identified three clusters that differed slightly from vaginally delivered infants, which were characterized by a high abundance of Bifidobacterium, high Clostridium and low Streptococcus and Ruminococcus genera, and high abundance of the family Enterobacteriaceae. Maternal dairy intake was associated with an increased odds of infants belonging to the high Clostridium cluster in infants born by Cesarean section (OR (95% CI) = 2.36 (1.05, 5.30)). Linear models suggested additional associations between maternal diet and infant intestinal microbes in both delivery mode strata.ConclusionsOur data indicate that maternal diet influences the infant gut microbiome and that these effects differ by delivery mode.

Effect of prenatal antioxidant intake on infants' respiratory infection is modified by a CD14 polymorphism.

Prenatal maternal diet may influence disease susceptibility in offspring with specific genetic backgrounds. We hypothesized that interactions between prenatal antioxidant intake and polymorphisms in immunity genes influence respiratory tract infection (RTI) susceptibility in infants at 12 months of age. This study included 550 infants. In the Cohort for Childhood Origin of Asthma and Allergic Diseases (COCOA) birth cohort study, prenatal maternal diet was assessed by administering a food frequency questionnaire. Infants' cord blood was genotyped for CD14 (rs2569190), TLR4 (rs1927911), and GSDMB (rs4794820) polymorphisms by the TaqMan method. Higher prenatal intake of total fruit and vegetables (FV) was associated with the decreased risk of RTI in offspring (P-trend=0.0430). In children with TT genotype at rs2569190, a higher prenatal intake of vitamins A and C, fruits, and total FV decreased RTI risk (P-trend <0.05), while in infants with TC+CC genotype, a higher prenatal intake of fruit increased RTI risk (P-trend <0.05). When analyzing the 3 genotypes, children with TT genotype at rs2569190 were more protected against RTIs compared with those with CC genotype with respect to vitamin C and fruits [odds ratio (OR)=5.04 and OR=10.30, respectively]. In children with CC genotype at rs1927911, RTI risk showed a dose-response association with a higher prenatal intake of vitamin C (P for interaction<0.05). A higher prenatal intake of fruits and total FV reduced RTI risk in infants with GA+AA genotype of rs4794820 (P for interaction<0.05). Prenatal antioxidant intake may reduce RTI risk in infants and this relationship may be modified by CD14, TLR4, and GSDMB polymorphisms.

Fast food consumption in pregnancy and subsequent asthma symptoms in young children.

Recent cross-sectional studies suggested children's current fast food consumption to be related to frequency of asthma and allergies. Maternal prenatal diet has been suspected to contribute to children's asthma and atopic disease risks. We hypothesized that maternal fast food intake during pregnancy increases offspring's risk for asthmatic symptoms. We conducted a population-based study of 1201 mother/child pairs in Los Angeles, California. Detailed information about prenatal fast food intake and other dietary, lifestyle/environmental factors, and pregnancy was collected shortly after birth; further data were retrieved from birth certificates. Using the International Study of Asthma and Allergies in Childhood core questions, asthma and rhinitis symptoms were assessed, and doctor's diagnoses were recorded in offspring 3.5 years after birth. Poisson regression with robust error variance using a log link function was used to estimate relative risks (RRs). Models were adjusted using covariates or propensity scores. Maternal prenatal fast food consumption related to increased relative risks of their children for severe, and current asthma symptoms (wheeze last 12 months combined with doctor's diagnosis) in a dose-dependent manner: 'once a month': RR: 0.99 (95% CI: 0.36, 2.75), 'once a week': 1.26 (0.47, 3.34); '3-4 days a week': 2.17 (0.77, 6.12); and 'every day' 4.46 (1.36 14.6) compared to 'never', adjusting for potential confounders (p for trend = 0.0025). There was also suggestion of increased risks for rhinitis symptoms. These findings suggest that in utero exposure to frequent fast food through maternal diet may be a risk factor for asthmatic symptoms in young children.

Impact of Prenatal Exposure to Humanized High Fat Diets on Murine Metabolic Phenotype

Prenatal exposures, including maternal diet, can alter risk for metabolic disease across the lifecourse. This study examines the effects of 2 prenatal high fat diets (HFDs) on mice offspring weight, nutrient utilization, and activity at 2 and 4 months of age. Two HFDs (43% fat kcal) were developed to mirror human intake: 1) Western (W) and 2) Mediterranean (M). Dams (n=44) were randomized to W, M, or Control (C) (7% fat) 2 wks prior to mating through pregnancy and lactation; pups were weaned onto C diet. One male (n=36) and 1 female (n=35) pup/litter were followed longitudinally with weekly weights and comprehensive phenotyping at 2 and 4 mos of age. ANOVA with Tukey's post-hoc analysis compared pups' mean metabolic outcomes across maternal prenatal diet groups. Prenatal HFD had a greater impact on females than males. M females were less ambulatory (p=0.046, 0.021) with less horizontal (p=0.023, 0.063) and vertical (p=0.035, 0.031) activity than C females at 2 and 4 mos, respectively. A similar trend was observed in 2 mo M males with less ambulatory (p=0.064) and horizontal (p=0.063) activity; by 4 mos, no activity differences were noted. At 4 mos, glucose oxidation (p=0.044) and respired CO2 (p=0.016) were lower in M females vs. C, consistent with increased utilization of fat as a primary fuel. All significant findings were during the light cycle, suggesting HFD impacts resting activity. MANOVA analysis found increased weight in M females but not males (p=0.047 and p=0.260). Thus, prenatal HFD alters female activity and nutrient utilization into early adulthood. A third round of phenotyping will be performed at 8 mos to characterize life course effects.

Deficient maternal zinc intake—but not folate—is associated with lower fetal heart rate variability

ObjectiveFew studies of maternal prenatal diet and child development examine micronutrient status in relation to fetal assessment. MethodsTwenty-four-hour dietary recall of zinc and folate and 20min of fetal heart rate were collected from 3rd trimester pregnant adolescents. ResultsDeficient zinc was associated with less fetal heart rate variability. Deficient folate had no associations with HRV. Neither deficient zinc nor deficient folate was related to fetal heart rate. ConclusionsThese findings, from naturalistic observation, are consistent with emerging data on prenatal zinc supplementation using a randomized control design. Practical ImplicationTaken together, the findings suggest that maternal prenatal zinc intake is an important and novel factor for understanding child ANS development.