13 research outputs found
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Risk of Micronutrient Inadequacy among Hispanic, Lactating Mothers: Preliminary Evidence from the Southern California Mother's Milk Study
Micronutrients are dietary components important for health and physiological function, and inadequate intake of these nutrients can contribute to poor health outcomes. The risk of inadequate micronutrient intake has been shown to be greater among low-income Hispanics and postpartum and lactating women. Therefore, we aimed to determine the risk of nutrient inadequacies based on preliminary evidence among postpartum, Hispanic women. Risk of micronutrient inadequacy for Hispanic women (29–45 years of age) from the Southern California Mother’s Milk Study (n = 188) was assessed using 24 h dietary recalls at 1 and 6 months postpartum and the estimated average requirement (EAR) fixed cut-point approach. Women were considered at risk of inadequate intake for a nutrient if more than 50% of women were consuming below the EAR. The Chronic Disease Risk Reduction (CDRR) value was also used to assess sodium intake. These women were at risk of inadequate intake for folate and vitamins A, D, and E, with 87.0%, 93.4%, 43.8%, and 95% of women consuming less than the EAR for these nutrients, respectively. Lastly, 71.7% of women consumed excess sodium. Results from this preliminary analysis indicate that Hispanic women are at risk of inadequate intake of important micronutrients for maternal and child health.
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Prenatal exposure to ambient air pollutants and early infant growth and adiposity in the Southern California Mother's Milk Study
Background
Prior epidemiological and animal work has linked in utero exposure to ambient air pollutants (AAP) with accelerated postnatal weight gain, which is predictive of increased cardiometabolic risk factors in childhood and adolescence. However, few studies have assessed changes in infant body composition or multiple pollutant exposures. Therefore, the objective of this study was to examine relationships between prenatal residential AAP exposure with infant growth and adiposity.
Methods
Residential exposure to AAP (particulate matter < 2.5 and 10 microns in aerodynamic diameter [PM2.5, PM10]; nitrogen dioxide [NO2]; ozone [O3]; oxidative capacity [Oxwt: redox-weighted oxidative potential of O3 and NO2]) was modeled by spatial interpolation of monitoring stations via an inverse distance-squared weighting (IDW2) algorithm for 123 participants from the longitudinal Mother’s Milk Study, an ongoing cohort of Hispanic mother-infant dyads from Southern California. Outcomes included changes in infant growth (weight, length), total subcutaneous fat (TSF; calculated via infant skinfold thickness measures) and fat distribution (umbilical circumference, central to total subcutaneous fat [CTSF]) and were calculated by subtracting 1-month measures from 6-month measures. Multivariable linear regression was performed to examine relationships between prenatal AAP exposure and infant outcomes. Models adjusted for maternal age, pre-pregnancy body mass index, socioeconomic status, infant age, sex, and breastfeeding frequency. Sex interactions were tested, and effects are reported for each standard deviation increase in exposure.
Results
NO2 was associated with greater infant weight gain (β = 0.14, p = 0.02) and TSF (β = 1.69, p = 0.02). PM10 and PM2.5 were associated with change in umbilical circumference (β = 0.73, p = 0.003) and TSF (β = 1.53, p = 0.04), respectively. Associations of Oxwt (pinteractions < 0.10) with infant length change, umbilical circumference, and CTSF were modified by infant sex. Oxwt was associated with attenuated infant length change among males (β = -0.60, p = 0.01), but not females (β = 0.16, p = 0.49); umbilical circumference among females (β = 0.92, p = 0.009), but not males (β = -0.00, p = 0.99); and CTSF among males (β = 0.01, p = 0.03), but not females (β = 0.00, p = 0.51).
Conclusion
Prenatal AAP exposure was associated with increased weight gain and anthropometric measures from 1-to-6 months of life among Hispanic infants. Sex-specific associations suggest differential consequences of in utero oxidative stress. These results indicate that prenatal AAP exposure may alter infant growth, which has potential to increase childhood obesity risk.
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Human milk oligosaccharide 2'-fucosyllactose links feedings at 1 month to cognitive development at 24 months in infants of normal and overweight mothers
Background
Infant cognitive development is influenced by maternal factors that range from obesity to early feeding and breast milk composition. Animal studies suggest a role for human milk oligosaccharide (HMO), 2’-fucosyllactose (2’FL), on learning and memory, yet no human studies have examined its impact on infant cognitive development relative to other HMOs and maternal factors.
Objective
To determine the impact of 2’FL from breast milk feeding on infant cognitive development at 24 months of age relative to maternal obesity and breast milk feeding frequency.
Methods and materials
Hispanic mother-infant pairs (N = 50) were recruited across the spectrum of pre-pregnancy BMI. Breast milk was collected at 1 and 6 months, and feedings/day were reported. Nineteen HMOs were analyzed using high-performance liquid chromatography, with initial interest in 2’FL. Infant cognitive development score was assessed with the Bayley-III Scale at 24 months. Linear regressions were used for prediction, and bootstrapping to determine mediation by 2’FL.
Results
Maternal pre-pregnancy BMI was not related to feedings/day or HMOs, but predicted poorer infant cognitive development (β = -0.31, P = 0.03). Feedings/day (β = 0.34) and 2’FL (β = 0.59) at 1 month predicted better infant cognitive development (both P≤ 0.01). The association of feedings/day with infant cognitive development was no longer significant after further adjustment for 2’FL (estimated mediation effect = 0.13, P = 0.04). There were no associations of feedings/day and 2’FL at 6 months with infant cognitive development.
Conclusions
Our findings suggest that maternal factors influence infant cognitive development through multiple means. Though maternal obesity may be a separate negative influence, greater frequency of breast milk feeding at 1 month contributed to infant cognitive development through greater exposure to 2’FL relative to other HMOs. The influence of 2’FL was not significant at 6 months, indicating that early exposure to 2’FL may be a critical temporal window for positively influencing infant cognitive development.
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PNPLA3 Genotype, Arachidonic Acid Intake, and Unsaturated Fat Intake Influences Liver Fibrosis in Hispanic Youth with Obesity
Non-alcoholic fatty liver disease impacts 15.2% of Hispanic adolescents and can progress to a build-up of scared tissue called liver fibrosis. If diagnosed early, liver fibrosis may be reversible, so it is necessary to understand risk factors. The aims of this study in 59 Hispanic adolescents with obesity were to: (1) identify potential biological predictors of liver fibrosis and dietary components that influence liver fibrosis, and (2) determine if the association between dietary components and liver fibrosis differs by PNPLA3 genotype, which is highly prevalent in Hispanic adolescents and associated with elevated liver fat. We examined liver fat and fibrosis, genotyped for PNPLA3 gene, and assessed diet via 24-h diet recalls. The prevalence of increased fibrosis was 20.9% greater in males, whereas participants with the GG genotype showed 23.7% greater prevalence. Arachidonic acid was associated with liver fibrosis after accounting for sex, genotype, and liver fat (β = 0.072, p = 0.033). Intakes of several dietary types of unsaturated fat have different associations with liver fibrosis by PNPLA3 genotype after accounting for sex, caloric intake, and liver fat. These included monounsaturated fat (βCC/CG = -0.0007, βGG = 0.03, p-value = 0.004), polyunsaturated fat (βCC/CG = -0.01, βGG = 0.02, p-value = 0.01), and omega-6 (βCC/CG = -0.0102, βGG = 0.028, p-value = 0.01). Results from this study suggest that reduction of arachidonic acid and polyunsaturated fatty acid intake might be important for the prevention of non-alcoholic fatty liver disease progression, especially among those with PNPLA3 risk alleles.
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Adverse Effects of Infant Formula Made with Corn-Syrup Solids on the Development of Eating Behaviors in Hispanic Children
Few studies have investigated the influence of infant formulas made with added corn-syrup solids on the development of child eating behaviors. We examined associations of breastmilk (BM), traditional formula (TF), and formula containing corn-syrup solids (CSSF) with changes in eating behaviors over a period of 2 years. Feeding type was assessed at 6 months in 115 mother–infant pairs. Eating behaviors were assessed at 12, 18 and 24 months. Repeated Measures ANCOVA was used to determine changes in eating behaviors over time as a function of feeding type. Food fussiness and enjoyment of food differed between the feeding groups (p p p p p < 0.01). Our findings suggest that Hispanic infants consuming CSSF may develop greater food fussiness and reduced enjoyment of food in the first 2 years of life compared to BM-fed infants
Early life gut microbiota is associated with rapid infant growth in Hispanics from Southern California.
We aimed to determine if the newborn gut microbiota is an underlying determinant of early life growth trajectories. 132 Hispanic infants were recruited at 1-month postpartum. The infant gut microbiome was characterized using 16S rRNA amplicon sequencing. Rapid infant growth was defined as a weight-for-age z-score (WAZ) change greater than 0.67 between birth and 12-months of age. Measures of infant growth included change in WAZ, weight-for-length z-score (WLZ), and body mass index (BMI) z-scores from birth to 12-months and infant anthropometrics at 12-months (weight, skinfold thickness). Of the 132 infants, 40% had rapid growth in the first year of life. Multiple metrics of alpha-diversity predicted rapid infant growth, including a higher Shannon diversity (OR = 1.83; 95% CI: 1.07-3.29; p = .03), Faith's phylogenic diversity (OR = 1.41, 95% CI: 1.05-1.94; p = .03), and richness (OR = 1.04, 95% CI: 1.01-1.08; p = .02). Many of these alpha-diversity metrics were also positively associated with increases in WAZ, WLZ, and BMI z-scores from birth to 12-months (pall<0.05). Importantly, we identified subsets of microbial consortia whose abundance were correlated with these same measures of infant growth. We also found that rapid growers were enriched in multiple taxa belonging to genera such as Acinetobacter, Collinsella, Enterococcus, Neisseria, and Parabacteroides. Moreover, measures of the newborn gut microbiota explained up to an additional 5% of the variance in rapid growth beyond known clinical predictors (R2 = 0.37 vs. 0.32, p < .01). These findings indicate that a more mature gut microbiota, characterized by increased alpha-diversity, at as early as 1-month of age, may influence infant growth trajectories in the first year of life
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Air pollution exposure is associated with the gut microbiome as revealed by shotgun metagenomic sequencing
Animal work indicates exposure to air pollutants may alter the composition of the gut microbiota. This study examined relationships between air pollutants and the gut microbiome in young adults residing in Southern California. Our results demonstrate significant associations between exposure to air pollutants and the composition of the gut microbiome using whole-genome sequencing. Higher exposure to 24-hour O3 was associated with lower Shannon diversity index, higher Bacteroides caecimuris, and multiple gene pathways, including L-ornithine de novo biosynthesis as well as pantothenate and coenzyme A biosynthesis I. Among other pollutants, higher NO2 exposure was associated with fewer taxa, including higher Firmicutes. The percent variation in gut bacterial composition that was explained by air pollution exposure was up to 11.2% for O3 concentrations, which is large compared to the effect size for many other covariates reported in healthy populations. This study provides the first evidence of significant associations between exposure to air pollutants and the compositional and functional profile of the human gut microbiome. These results identify O3 as an important pollutant that may alter the human gut microbiome