Dataset Information

Calories, Caffeine and the Onset of Obesity in Young Children.

ABSTRACT:

Objective

High calorie foods and beverages, which often contain caffeine, contribute to child overweight/obesity. We evaluated the results of an educational intervention to promote healthy growth in very young children. Secondarily, we used detailed diet data to explore the association of nutrient intake with the early development of overweight and obesity.

Methods

Mothers were obese Latina women, enrolled prenatally, and their infants. Specially trained community health workers provided breastfeeding support and nutrition education during 10 home visits, birth to 24 months. At follow-up, age 18 to 36 months, we measured growth and completed detailed diet recalls (1-7 recall days/child).

Results

Of 174 infants randomized, 106 children were followed for 24 to 36 months. The educational intervention did not prevent overweight/obesity. Forty-two percent of children became overweight or obese. Fifty-eight percent of children consumed caffeine on at least 1 recall day. Mean intake was 0.48 mg/kg/day. Caffeine correlated with higher consumption of calories, and added sugar and decreased intake of protein, fiber and dairy. Compared with days without caffeine, on days when caffeine was consumed, children ingested 121 more calories and 3.8 gm less protein. Children frequently consumed less than the recommended daily intake of key nutrients such as fiber, vegetables, whole fruit, and vitamins.

Conclusions

Caffeine was a marker for increased intake of calories and decreased intake of key nutrients. When discussing dietary intake in early childhood, practitioners should screen for nutrient deficiency in young children and recommend limiting the intake of caffeinated foods and beverages.

SUBMITTER: McCormick DP

PROVIDER: S-EPMC7416448 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesTo assess whether epigenetic mechanisms affecting gene expression may be involved in the pathogenesis of early-onset myopia, we performed genome-wide DNA methylation analyses of umbilical cord tissues, and assessed any associations between CpG site-specific methylation and the development of the disorder when the children were 3 years old.MethodsGenome-wide DNA methylation profiling of umbilical cord samples from 519 Singaporean infants involved in a prospective birth cohort 'Growing Up in Singapore Towards healthy Outcomes' (GUSTO) was performed using the Illumina Infinium HumanMethylation450K chip microarray. Multivariable logistic regression models were used to assess any associations between site-specific CpG methylation of umbilical cord tissue at birth and myopia risk in 3 year old children, adjusting for potential confounders. Gene expression of genes located near CpG sites that demonstrated statistically significant associations were measured in relevant ocular tissues using human and mouse fetal and adult eye samples.ResultsWe identified statistically significant associations between DNA methylation levels at five CpG sites and early-onset myopia risk after correcting for multiple comparisons using a false discovery rate of 5%. Two statistically significant CpG sites were identified in intergenic regions: 8p23(p = 1.70×10-7) and 12q23.2(p = 2.53×10-7). The remaining 3 statistically significant CpG sites were identified within the following genes: FGB (4q28, p = 3.60×10-7), PQLC1 (18q23, p = 8.9×10-7) and KRT12 (17q21.2, p = 1.2×10-6). Both PQLC1 and KRT12 were found to be significantly expressed in fetal and adult cornea and sclera tissues in both human and mouse.ConclusionsWe identified five CpG methylation sites that demonstrate a statistically significant association with increased risk of developing early-onset myopia. These findings suggest that variability in the neonatal cord epigenome may influence early-onset myopia risk in children. Further studies of the epigenetic influences on myopia risk in larger study populations, and the associations with adulthood myopia risk are warranted.