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 < 0.05) and changed over time for CSSF and TF (p < 0.01). Food fussiness increased from 12 to 18 and 12 to 24 months for CSSF and from 12 to 24 months for TF (p < 0.01), while it remained stable for BM. Enjoyment of food decreased from 12 to 24 months for CSSF (p < 0.01), while it remained stable for TF and BM. There was an interaction between feeding type and time for food fussiness and enjoyment of food (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.

Clinical Intervention to Reduce Dietary Sugar Does Not Affect Liver Fat in Latino Youth, Regardless of PNPLA3 Genotype: A Randomized Controlled Trial.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) among Latinos is partially attributed to a prevalent C>G polymorphism in the patatin-like phospholipase 3 (PNPLA3) gene. Cross-sectional analyses in Latino children showed the association between dietary sugar and liver fat was exacerbated by GG genotype. Pediatric feeding studies show extreme sugar restriction improves liver fat, but no prior trial has examined the impact of a clinical intervention or whether effects differ by PNPLA3 genotype. OBJECTIVES: We aimed to test effects of a clinical intervention to reduce dietary sugar compared with standard dietary advice on change in liver fat, and secondary-endpoint changes in liver fibrosis, liver enzymes, and anthropometrics; and whether effects differ by PNPLA3 genotype (assessed retrospectively) in Latino youth with obesity (BMI ≥ 95th percentile). METHODS: This parallel-design trial randomly assigned participants (n = 105; mean baseline liver fat: 12.7%; mean age: 14.8 y) to control or sugar reduction (goal of ≤10% of calories from free sugar) for 12 wk. Intervention participants met with a dietitian monthly and received delivery of bottled water. Changes in liver fat, by MRI, were assessed by intervention group via general linear models. RESULTS: Mean free sugar intake decreased in intervention compared with control [11.5% to 7.3% compared with 13.9% to 10.7% (% energy), respectively; P = 0.02], but there were no significant effects on liver outcomes or anthropometrics (Pall > 0.10), and no PNPLA3 interactions (Pall > 0.10). In exploratory analyses, participants with whole-body fat mass (FM) reduction (mean ± SD: -1.9 ± 2.4 kg), irrespective of randomization, had significant reductions in liver fat compared with participants without FM reduction (median: -2.1%; IQR: -6.5% to -0.8% compared with 0.3%; IQR: -1.0% to 1.1%; P < 0.001). CONCLUSIONS: In Latino youth with obesity, a dietitian-led sugar reduction intervention did not improve liver outcomes compared with control, regardless of PNPLA3 genotype. Results suggest FM reduction is important for liver fat reduction, confirming clinical recommendations of weight loss and a healthy diet for pediatric NAFLD.This trial was registered at clinicaltrials.gov as NCT02948647.

Associations of maternal non-nutritive sweetener intake during pregnancy with offspring body mass index and body fat from birth to adolescence.

BACKGROUND/OBJECTIVE: The evidence that maternal non-nutritive sweetener (NNS) intake during pregnancy increases childhood obesity risk is conflicting. A potential reason for this is that all prior studies examined childhood body mass index (BMI) at only one timepoint and at different ages. We examined the extent to which NNS intake during pregnancy is associated with offspring BMI z-score and body fat longitudinally from birth to 18 years. SUBJECTS: A total of 1683 children from Project Viva, a prospective pre-birth cohort, were recruited from 1999 to 2002 in Massachusetts. METHODS: We assessed maternal NNS intake in the first and second trimesters of pregnancy using a semiquantitative food frequency questionnaire. Our outcomes were offspring BMI z-score, (at birth, infancy (median 6.3 months), early childhood (3.2 years), mid-childhood (7.7 years), and early adolescence (12.9 years)), sum of skinfolds (SS), fat mass index (FMI) measured by dual x-ray absorptiometry, and BMI z-score trajectory from birth to 18 years. We adjusted models for maternal pre-pregnancy BMI, age, race/ethnicity, education, parity, pre-pregnancy physical activity, smoking, and paternal BMI and education. RESULTS: A total of 70% of mothers were white and pre-pregnancy BMI was 24.6 ± 5.2 kg/m2. The highest quartile of NNS intake (Q4: 0.98 ± 0.91 servings/day) was associated with higher BMI z-score in infancy (ß 0.20 units; 95% CI 0.02, 0.38), early childhood (0.21; 0.05, 0.37), mid-childhood (0.21; 0.02, 0.40), and early adolescence (0.14; -0.07, 0.35) compared with Q1 intake (Q1: 0.00 ± 0.00 servings/day). Q4 was also associated with higher SS in early childhood (1.17 mm; 0.47, 1.88), mid-childhood (2.33 mm; 0.80, 3.87), and early adolescence (2.27 mm; -0.06, 4.60) and higher FMI in mid-childhood (0.26 kg/m2; -0.07, 0.59). Associations of maternal NNS intake with offspring BMI z-score became stronger with increasing age from 3 to 18 years (Pinteraction < 0.0001). CONCLUSIONS: Maternal NNS intake during pregnancy is associated with increased childhood BMI z-score and body fat from birth to teenage years. This is relevant given the escalating obesity epidemic, and popularity of NNS.

Development and Validation of a Prediction Model for Infant Fat Mass.

OBJECTIVES: To develop and validate a prediction model for fat mass in infants ≤12 kg using easily accessible measurements such as weight and length. STUDY DESIGN: We used data from a pooled cohort of 359 infants age 1-24 months and weighing 3-12 kg from 3 studies across Southern California and New York City. The training data set (75% of the cohort) included 269 infants and the testing data set (25% of the cohort) included 90 infants age 1-24 months. Quantitative magnetic resonance was used as the standard measure for fat mass. We used multivariable linear regression analysis, with backwards selection of predictor variables and fractional polynomials for nonlinear relationships to predict infant fat mass (from which lean mass can be estimated by subtracting resulting estimates from total mass) in the training data set. We used 5-fold cross-validation to examine overfitting and generalizability of the model's predictive performance. Finally, we tested the adjusted model on the testing data set. RESULTS: The final model included weight, length, sex, and age, and had high predictive ability for fat mass with good calibration of observed and predicted values in the training data set (optimism-adjusted R2: 92.1%). Performance on the test dataset showed promising generalizability (adjusted R2: 85.4%). The mean difference between observed and predicted values in the testing dataset was 0.015 kg (-0.043 to -0.072 kg; 0.7% of the mean). CONCLUSIONS: Our model accurately predicted infant fat mass and could be used to improve the accuracy of assessments of infant body composition for effective early identification, surveillance, prevention, and management of obesity and future chronic disease risk.

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.

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.

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 (ß = 0.14, p = 0.02) and TSF (ß = 1.69, p = 0.02). PM10 and PM2.5 were associated with change in umbilical circumference (ß = 0.73, p = 0.003) and TSF (ß = 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 (ß = -0.60, p = 0.01), but not females (ß = 0.16, p = 0.49); umbilical circumference among females (ß = 0.92, p = 0.009), but not males (ß = -0.00, p = 0.99); and CTSF among males (ß = 0.01, p = 0.03), but not females (ß = 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.

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 (ß = 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 (ßCC/CG = -0.0007, ßGG = 0.03, p-value = 0.004), polyunsaturated fat (ßCC/CG = -0.01, ßGG = 0.02, p-value = 0.01), and omega-6 (ßCC/CG = -0.0102, ßGG = 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.

Specific amino acids but not total protein attenuate postpartum weight gain among Hispanic women from Southern California.

There is a high prevalence of obesity and type 2 diabetes in the United States, particularly among Hispanic women, which may be partly explained by failure to lose gestational weight during the postpartum period. Previous work indicates that protein and amino acids may protect against weight gain; therefore, this study examined the impact of dietary protein and amino acid intake on changes in postpartum weight and the percent of women meeting the Estimated Average Requirement (EAR) for these dietary variables among Hispanic women from the Southern California Mother's Milk Study (n = 99). Multivariable linear regression analysis was used to examine the associations between protein and amino acid intake with change in weight after adjusting for maternal age, height, and energy intake. Women's weight increased from prepregnancy to 1-month and 6-months postpartum (71.1 ± 14.6 vs. 73.1 ± 13.1 vs. 74.5 ± 14.6 kg, p < .0001). Although dietary protein was not associated with weight change (ß = -1.09; p = .13), phenylalanine (ß = -1.46; p = .04), tryptophan (ß = -1.71; p = .009), valine (ß = -1.34; p = .04), isoleucine (ß = -1.26; p = .045), and cysteine (ß = -1.52; p = .02) intake were inversely associated with weight change. Additionally, fewer women met the EAR values for cysteine (11.1%), phenylalanine (60.6%), and methionine (69.7%), whereas most women met the EAR values for tryptophan (92.9%), valine (96.0%), and isoleucine (94.9%). Study results indicate that several essential and conditionally essential amino acids were associated with postpartum weight loss, with a significant portion of women not meeting recommended intake levels for some of these amino acids. These results highlight the importance of postpartum maternal diet as a potential modifiable risk factor.

Human Milk Exosomal MicroRNA: Associations with Maternal Overweight/Obesity and Infant Body Composition at 1 Month of Life.

Among all the body fluids, breast milk is one of the richest sources of microRNAs (miRNAs). MiRNAs packaged within the milk exosomes are bioavailable to breastfeeding infants. The role of miRNAs in determining infant growth and the impact of maternal overweight/obesity on human milk (HM) miRNAs is poorly understood. The objectives of this study were to examine the impact of maternal overweight/obesity on select miRNAs (miR-148a, miR-30b, miR-29a, miR-29b, miR-let-7a and miR-32) involved in adipogenesis and glucose metabolism and to examine the relationship of these miRNAs with measures of infant body composition in the first 6 months of life. Milk samples were collected from a cohort of 60 mothers (30 normal-weight [NW] and 30 overweight [OW]/obese [OB]) at 1-month and a subset of 48 of these at 3 months of lactation. Relative abundance of miRNA was determined using real-time PCR. The associations between the miRNAs of interest and infant weight and body composition at one, three, and six months were examined after adjusting for infant gestational age, birth weight, and sex. The abundance of miR-148a and miR-30b was lower by 30% and 42%, respectively, in the OW/OB group than in the NW group at 1 month. miR-148a was negatively associated with infant weight, fat mass, and fat free mass, while miR-30b was positively associated with infant weight, percent body fat, and fat mass at 1 month. Maternal obesity is negatively associated with the content of select miRNAs in human milk. An association of specific miRNAs with infant body composition was observed during the first month of life, suggesting a potential role in the infant's adaptation to enteral nutrition.

Longitudinal Changes in Human Milk Oligosaccharides (HMOs) Over the Course of 24 Months of Lactation.

BACKGROUND: Human milk oligosaccharides (HMOs) are complex glycans that are highly abundant in human milk. While over 150 HMOs have been identified, it is unknown how individual HMOs change in concentration over 24 months of lactation. OBJECTIVES: To understand how HMO concentrations change over 24 months of lactation. METHODS: Breast milk samples were collected from participants in a longitudinal cohort study of Hispanic mother-infant pairs at 1, 6, 12, 18, and 24 months postpartum. Concentrations of 19 of the most abundant HMOs were measured using HPLC. Because the parent study is ongoing and not all participants have finished all time points yet, the sample sizes ranged per time point (n = 207 at 1 month; n = 109 at 6 months; n = 83 at 12 months; n = 59 at 18 months; and n = 28 at 24 months). Approximately 88% of participants were classified as HMO secretors-a genetic factor that affects concentrations of HMOs such as 2'fucosyllactose (2'FL) and lacto-N-fucopentaose I-while the remaining 12% were classified as nonsecretors. Mixed models were used to examine changes in HMO concentrations and relative abundances over the course of lactation. RESULTS: The majority of HMOs significantly decreased in concentration over the course of lactation. The exceptions were 2'FL, sialyl-lacto-N-tetraose b, and disialyl-lacto-N-tetraose, which did not change with time, and 3-fucosyllactose (3FL) and 3'-sialyllactose (3'SL), which significantly increased. The concentration of 3FL increased 10-fold, from 195 (IQR 138-415) µg/mL at 1 month to 1930 (1100-2630) µg/mL at 24 months, while 3'SL increased 2-fold, from 277 (198-377) µg/mL to 568 (448-708) µg/mL over the same time period. CONCLUSIONS: These results indicate that HMOs do not decrease in concentration uniformly across lactation. In particular, 3FL and 3'SL increased over the course of lactation in this cohort. Future studies are required to fully understand the functions of these HMOs.

Interleukin-1 Receptor-1 Deficiency Impairs Metabolic Function in Pregnant and Non-Pregnant Female Mice.

SCOPE: Glucose intolerance during pregnancy is associated with short- and long-term maternal and offspring health consequences. In young male mice, knockout of the major pro-inflammatory mediator interleukin-1-receptor-1 (IL1R1) protects against high-fat diet (HFD)-induced glucose intolerance and metabolic dysfunction. This phenotype has not been examined during pregnancy. The hypothesis that IL1R1 depletion will protect females against HFD-induced glucose intolerance and metabolic dysfunction before, during, and post pregnancy is tested. METHODS AND RESULTS: C57BL/6J control and IL1R1 knockout (IL1R1-/- ) mice are randomized to either a control diet (10% kcal from fat) or HFD (45% kcal from fat), and three distinct cohorts are established: nulliparous, pregnant, and postpartum females. Contrary to the authors' hypothesis, it is found that IL1R1-/- does not protect against glucose intolerance in nulliparous or pregnant females, and while control HFD animals see a resolution of glucose tolerance postpartum, IL-1R1-/- mice remain impaired. These effects are accompanied by adipocyte hypertrophy, hyperleptinemia, and increased adipose tissue inflammatory gene expression. Maternal genotype differentially affects fetal growth in male and female fetuses, demonstrating sexual dimorphism in this genotype prior to birth. CONCLUSIONS: These findings suggest that IL1R1 signaling is important for normal metabolic functioning in females, during and outside of pregnancy.

Timing of food consumption in Hispanic adolescents with obesity.

BACKGROUND: Little is known about the normal eating time periods in adolescents with obesity and how these patterns change throughout development. As the obesity epidemic continues to rise in adolescence, it becomes imperative to understand developmentally appropriate eating behaviours and to create weight management strategies that build on those innate patterns and preferences. The purpose of this study was to determine the most common habitual eating windows observed in adolescents with obesity. METHODS: Participants were 101 Hispanic adolescents (mean age 14.8 ± 2.1 years; 48 male/53 female) with obesity (BMI ≥95th percentile) who were recruited as part of a larger clinical trial. Dietary intake and meal timing was determined using multiple pass 24-hours recalls. Histograms were utilized to determine the natural distribution of percent consumption of total kilocalories, carbohydrates and added sugar per hour. RESULTS: The majority of total kilocalories (65.4%), carbohydrates (65.3%) and added sugar (59.1%) occurred between 11:00 and 19:00. Adolescents were 2.5 to 2.9 times more likely to consume kilocalories, carbohydrates, and added sugar during the 8-hour window between 11:00 am and 19:00 pm than other time windows examined (all P < .001). The consumption of these calories did not differ between weekdays and weekend (P > .05) or by sex. CONCLUSIONS: In this cohort, more than 60% of calories, carbohydrates and added sugar were consumed between 11:00 am and 19:00 pm, which is concordant with an afternoon/evening chronotype that is common in adolescents. Our findings support this 8-hour period as a practical window for weight loss interventions that target pre-specified eating periods in this population.

Associations of maternal fructose and sugar-sweetened beverage and juice intake during lactation with infant neurodevelopmental outcomes at 24 months.

BACKGROUND: Our prior studies revealed that infant somatic growth is influenced by fructose in breast milk, and fructose in breast milk is increased in response to maternal sugar-sweetened beverage (SSB) intake in lactation. It is unknown whether infant neurodevelopmental outcomes are also influenced by maternal SSBs in lactation. OBJECTIVES: To determine whether infant cognitive development at 24 postnatal months was influenced by maternal fructose consumption during lactation, and whether this relation persisted after accounting for maternal SSB and juice (SSB + J) intake. METHODS: Hispanic mother-infant pairs (n = 88) were recruited across the spectrum of prepregnancy BMI. Mothers completed two 24-h dietary recalls at 1 and 6 postnatal months, and reported breastfeedings per day. The Bayley-III Scales of Infant Development were administered at 24 postnatal months to assess infant cognition. Linear regressions were used to examine associations, reported as unstandardized (B) coefficients, 95% CIs, and P values. RESULTS: Mothers consumed 1656 ± 470 kcal, 21.8 ± 12 g fructose, and 2.5 ± 2.6 servings SSBs + J, and reported 6.9 ± 2.1 breastfeedings per day at 1 postnatal month. Controlling for maternal age, prepregnancy BMI, education level, kilocalories, infant age, sex, and birthweight revealed that infant cognitive development scores at 24 postnatal months correlated inversely with maternal fructose consumption at 1 postnatal month (B = -0.08; 95% CI = -0.13, -0.03; P < 0.01). The association of infant cognitive development scores with maternal fructose consumption was no longer significant after adjustment for maternal SSB + J intake (B = -0.05; 95% CI = -0.10, 0.00; P = 0.07), whereas maternal SSB + J intake was significant in the same model (B = -0.29; 95% CI = -0.52, -0.05; P = 0.02). Infant cognitive development scores were not associated with maternal fructose and SSB + J consumption at 6 postnatal months. CONCLUSIONS: Our findings suggest that infant neurodevelopmental outcomes at 24 postnatal months can be adversely influenced by maternal fructose intake in early lactation, and this could be attributed to maternal SSB + J intake.

Lactose-reduced infant formula with added corn syrup solids is associated with a distinct gut microbiota in Hispanic infants.

Infant formula feeding, compared with human milk, has been associated with development of a distinct infant gut microbiome, but no previous study has examined effects of formula with added sugars. This work examined differences in gut microbiota among 91 Hispanic infants who consumed human milk [at breast (BB) vs. pumped in bottle (BP)] and 2 kinds of infant formula [(traditional lactose-based (TF) vs. lactose-reduced with added sugar (ASF)]. At 1 and 6 months, infant stool was collected to characterize gut microbiota. At 6 months, mothers completed 24-hour dietary recalls and questionnaires to determine infant consumption of human milk (BB vs. BP) or formula (TF vs. ASF). Linear regression models were used to determine associations of milk consumption type and microbial features at 6 months. Infants in the formula groups exhibited a significantly more 'mature' microbiome than infants in the human milk groups with the most pronounced differences observed between the ASF vs. BB groups. In the ASF group, we observed reduced log-normalized abundance of Bifidobacteriaceae (TF-BB Mean Difference = -0.71, ASF-BB Mean Difference = -1.10), and increased abundance of Lachnospiraceae (TF-BB Mean Difference = +0.89, ASF-BB Mean Difference = +1.20). We also observed a higher Community Phenotype Index of propionate, most likely produced by Lachnospiraceae, in the ASF group (TF-BB Mean Difference = +0.27, ASF-BB Mean Difference = +0.36). This study provides the first evidence that consumption of infant formula with added sugar may have a stronger association than birth delivery mode, infant caloric intake, and maternal BMI on the infant's microbiome at 6 months of age.

Human Milk Oligosaccharides and Hispanic Infant Weight Gain in the First 6 Months.

OBJECTIVE: The aim of this study was to determine whether human milk oligosaccharides (HMOs) at 1 month predicted infant weight gain at 6 months and whether associations varied by HMO secretor status. METHODS: Participants were 157 Hispanic mother-infant pairs. Human milk samples were collected at 1 month. Nineteen individual HMOs were analyzed using high-performance liquid chromatography, and secretor status was determined by the presence of 2'-fucosyllactose or lacto-N-fucopentaose (LNFP) I. Infant weight was measured at 1 and 6 months. Path analysis was used to test effects of HMO composition on infant weight gain, adjusting for maternal age, prepregnancy BMI, and infant age, sex, and birth weight. RESULTS: In the total sample, higher LNFPII predicted lower infant weight gain (g1 = -4.1, P = 0.004); this was observed in both nonsecretor (g1 = -3.0, P = 0.006) and secretor groups (g1 = -4.7, P = 0.014). In the nonsecretor group, higher lacto-N-neotetraose (g1 = 7.6, P = 0.011) and disialyllacto-N-tetraose (g1 = 14.3, P = 0.002) predicted higher infant weight gain. There were no other associations in the secretor group. CONCLUSIONS: Our data suggest that higher LNFPII in human milk may decrease obesity risk across all infants, whereas higher lacto-N-neotetraose and disialyllacto-N-tetraose may increase obesity risk in infants of nonsecretors only.

Interleukin 1 Receptor 1 Knockout and Maternal High Fat Diet Exposure Induces Sex-Specific Effects on Adipose Tissue Adipogenic and Inflammatory Gene Expression in Adult Mouse Offspring.

Background: The global incidence of obesity continues to rise, increasing the prevalence of metabolic diseases such as insulin resistance, dyslipidemia, and type 2 diabetes mellitus. Low-grade chronic inflammation, associated with the obese state, also contributes to the development of these metabolic comorbidities. Interleukin-1-receptor-1 (IL-1R1), a pro-inflammatory mediator, bridges the metabolic and inflammatory systems. In young male mice, deficiency of IL-1R1 (IL-1R1-/-) paired with a high-fat diet (HFD) offered beneficial metabolic effects, however in female mice, the same pairing led to metabolic dysfunction. Therefore, we examined the contribution of maternal HFD in combination with IL1R1-/- to metabolic health in adult offspring. Methods: Female C57BL/6 and IL-1R1-/- mice were randomly assigned to a control diet (10% kcal from fat) or HFD (45% kcal from fat) 10 days prior to mating and throughout gestation and lactation. Male and female offspring were housed in same-sex pairs post-weaning and maintained on control diets until 16 weeks old. At 15 weeks, an oral glucose tolerance test (OGTT) was performed to assess glucose tolerance. Histological analysis was carried out to assess adipocyte size and gene expression of adipogenic and inflammatory markers were examined. Results: IL-1R1-/- contributed to increased body weight in male and female adult offspring, irrespective of maternal diet. IL-1R1-/- and maternal HFD increased adipocyte size in the gonadal fat depot of female, but not male offspring. In female offspring, there was reduced expression of genes involved in adipogenesis and lipid metabolism in response to IL1R1-/- and maternal HFD. While there was an increase in inflammatory gene expression in response to maternal HFD, this appeared to be reversed in IL1R1-/- female offspring. In male offspring, there was no significant impact on adipogenic or lipid metabolism pathways. There was an increase in inflammatory gene expression in IL1R1-/- male offspring from HFD-fed mothers. Conclusion: This study suggests that IL-1R1 plays a complex and important role in the metabolic health of offspring, impacting adipogenesis, lipogenesis, and inflammation in a sex-specific manner.

Associations between human milk oligosaccharides (HMOs) and eating behaviour in Hispanic infants at 1 and 6 months of age.

BACKGROUND: Human milk oligosaccharides (HMOs) are naturally occurring glycans in human breast milk that act as prebiotics in the infant gut. Prebiotics have been demonstrated to suppress appetite in both adults and children. Therefore, HMOs may affect infant eating behaviour. OBJECTIVE: To determine if HMOs in breast milk are associated with eating behaviour in Hispanic infants. METHODS: Cross-sectional analysis of a prospective cohort of Hispanic mother-infant dyads (1-month, n = 157; 6-months, n = 69). Breast milk samples were screened for 19 HMOs using high pressure liquid chromatography, and eating behaviour was assessed using the Baby Eating Behaviour Questionnaire (BEBQ). We conducted multiple linear regressions to examine associations between HMOs and BEBQ scores, adjusted for maternal pre-pregnancy BMI, infant sex, birthweight, delivery mode and number of breastfeedings per day. We stratified by HMO secretor status-a genetic determinant of the types of HMOs produced. RESULTS: At 1 month, LNnT (lacto-N-neotetraose; P = .04) was negatively associated with food responsiveness in the total sample, while DFLNT (difucosyllacto-N-tetrose; P = .03) and DSLNT (disialyl-LNT; P = .04) were negatively associated with food responsiveness in secretors only. At 6 months, LSTc (sialyllacto-N-tetraose c; P = .01), FLNH (fucosyllacto-N-hexaose; P = .03), LNH (lacto-N-hexaose; P = .006) and DSLNH (disialyllacto-N-hexaose; P = .05) were positively associated with food responsiveness in both the total sample and secretors only. CONCLUSIONS: We found several HMOs that were both positively and negatively associated with infant food responsiveness, which is a measure of drive to eat.

Added sugar and sugar-sweetened beverages are associated with increased postpartum weight gain and soluble fiber intake is associated with postpartum weight loss in Hispanic women from Southern California.

BACKGROUND: Obesity prevalence remains high in the United States, and there is an increased risk among women who do not lose their gestational weight gain during the postpartum period. Indicators of dietary carbohydrate quality including added sugar consumption, glycemic load, and glycemic index have been linked with weight gain, whereas fiber may protect against obesity. However, these dietary factors have not been examined during the postpartum period. OBJECTIVES: The aim of this study was to determine whether dietary sugars and fiber intake were associated with changes in postpartum weight. METHODS: We examined Hispanic women from the longitudinal Southern California Mother's Milk Study (n = 99) at 1 and 6 mo postpartum. Maternal assessments included height, weight, and dietary intake based on 24-h diet recalls. We used multivariable linear regression to examine the relation between maternal diet and change in postpartum weight after adjusting for maternal age, height, and energy intake. RESULTS: Higher intake of added sugar was associated with postpartum weight gain (ß: 0.05; 95% CI: 0.004, 0.10; P = 0.05). In addition, a half 8-ounce (8 fluid ounces = 236.6 mL) serving per day increase in soft drinks was associated with a 1.52-kg increase in weight (95% CI: 0.70, 2.34 kg; P < 0.001). A high glycemic index (ß: 0.25; 95% CI: 0.07, 0.42; P = 0.006) and glycemic load (ß: 0.04; 95% CI: 0.002, 0.08; P = 0.04) were associated with postpartum weight gain. Higher soluble fiber was associated with a decrease in postpartum weight (ß: -0.82 kg; 95% CI: -1.35, -0.29 kg; P = 0.003) and the negative effects of added sugar, sugary beverages, and high-glycemic-index and -load diets were partially attenuated after adjusting for soluble fiber intake. CONCLUSIONS: Increased consumption of added sugar, sugar-sweetened beverages, and high-glycemic diets were associated with greater weight gain in the first 6 mo postpartum. In addition, increased consumption of soluble fiber was associated with postpartum weight loss, which may partially offset the obesogenic effects of some dietary sugars.

Carbohydrate composition in breast milk and its effect on infant health.

PURPOSE OF REVIEW: This narrative review presents the current state of available evidence regarding the role of breast milk carbohydrates on infant outcomes, with a primary focus on growth and body composition. RECENT FINDINGS: To date, there is a paucity of available data that exists in this realm. The current literature focuses on the role of two carbohydrate fractions in breast milk, and their relationships with infant outcomes in the first six months of life: oligosaccharides and fructose. A small but growing body of research indicates robust associations of both oligosaccharides and fructose in breast milk with infant weight and length, as well as bone, fat, and lean mass. There is also emerging evidence to support the role of these same carbohydrate fractions in breast milk in infant cognitive development. SUMMARY: The present state of the science suggests that oligosaccharides and fructose in breast milk play a role in infant growth and body composition and introduces intriguing associations of these two carbohydrate fractions with infant cognitive development as well.